Gene Symbol: c-Met
Description: MET proto-oncogene, receptor tyrosine kinase
Alias: AUTS9, DFNB97, HGFR, RCCP2, c-Met, hepatocyte growth factor receptor, HGF receptor, HGF/SF receptor, SF receptor, proto-oncogene c-Met, scatter factor receptor, tyrosine-protein kinase Met
Species: human
Products:     c-Met

Top Publications

  1. Hu Z, Lin Y, Chen H, Mao Y, Wu J, Zhu Y, et al. MicroRNA-101 suppresses motility of bladder cancer cells by targeting c-Met. Biochem Biophys Res Commun. 2013;435:82-7 pubmed publisher
    ..In conclusion, we have shown miR-101 to be a novel suppressor of T24 cell migration and invasion through its negative regulation of c-Met. ..
  2. Hagman Z, Haflidadóttir B, Ansari M, Persson M, Bjartell A, Edsjö A, et al. The tumour suppressor miR-34c targets MET in prostate cancer cells. Br J Cancer. 2013;109:1271-8 pubmed publisher
    ..These findings provide a novel molecular mechanism of MET regulation in PCa and contribute to the increasing evidence that miR-34c has a key tumour suppressive role in PCa. ..
  3. Leiser D, Pochon B, Blank Liss W, Francica P, Glück A, Aebersold D, et al. Targeting of the MET receptor tyrosine kinase by small molecule inhibitors leads to MET accumulation by impairing the receptor downregulation. FEBS Lett. 2014;588:653-8 pubmed publisher
    ..These data may suggest careful consideration for design of anti-MET clinical protocols. ..
  4. Varkaris A, Gaur S, Parikh N, Song J, Dayyani F, Jin J, et al. Ligand-independent activation of MET through IGF-1/IGF-1R signaling. Int J Cancer. 2013;133:1536-46 pubmed publisher
    ..The results further suggest that MET may be activated by multiple receptor tyrosine kinase receptors, and dual targeting of these receptors may be important therapeutically. ..
  5. Ha S, Lee J, Kang S, Do I, Ahn S, Park J, et al. MET overexpression assessed by new interpretation method predicts gene amplification and poor survival in advanced gastric carcinomas. Mod Pathol. 2013;26:1632-41 pubmed publisher
    ..MET overexpression is an independent prognostic factor and could be a potential target and predictor of benefit for targeted therapy with MET inhibitors. ..
  6. Xu X, Chen H, Lin Y, Hu Z, Mao Y, Wu J, et al. MicroRNA-409-3p inhibits migration and invasion of bladder cancer cells via targeting c-Met. Mol Cells. 2013;36:62-8 pubmed publisher
    ..We further showed that MMP2 and MMP9 may be downstream effector proteins of miR-409-3p. These findings indicate that miR-409-3p could be a potential tumor suppressor in bladder cancer. ..
  7. Troiani T, Martinelli E, Napolitano S, Vitagliano D, Ciuffreda L, Costantino S, et al. Increased TGF-? as a mechanism of acquired resistance to the anti-EGFR inhibitor cetuximab through EGFR-MET interaction and activation of MET signaling in colon cancer cells. Clin Cancer Res. 2013;19:6751-65 pubmed publisher
    ..The combined inhibition of EGFR and MET receptor could represent a strategy for preventing and/or overcoming cetuximab resistance in patients with colorectal cancer. ..
  8. Li L, Puliyappadamba V, Chakraborty S, Rehman A, Vemireddy V, Saha D, et al. EGFR wild type antagonizes EGFRvIII-mediated activation of Met in glioblastoma. Oncogene. 2015;34:129-134 pubmed publisher
  9. Liu Y, Shen D, Yin X, Gavine P, Zhang T, Su X, et al. HER2, MET and FGFR2 oncogenic driver alterations define distinct molecular segments for targeted therapies in gastric carcinoma. Br J Cancer. 2014;110:1169-78 pubmed publisher
    ..A significant proportion of HER2-negative patients may potentially benefit from MET- or FGFR2-targeted therapies. ..

More Information

Publications166 found, 100 shown here

  1. Wang X, DeFrances M, Dai Y, Pediaditakis P, Johnson C, Bell A, et al. A mechanism of cell survival: sequestration of Fas by the HGF receptor Met. Mol Cell. 2002;9:411-21 pubmed
    ..Our results describe a direct link between growth factor tyrosine kinase receptors and death receptors to establish a novel paradigm in growth regulation. ..
  2. Tulasne D, Deheuninck J, Lourenco F, Lamballe F, Ji Z, Leroy C, et al. Proapoptotic function of the MET tyrosine kinase receptor through caspase cleavage. Mol Cell Biol. 2004;24:10328-39 pubmed
    ..Finally, HGF/SF treatment does not favor MET cleavage and apoptosis, confirming the known survival role of ligand-activated MET. Our results show that stress stimuli convert the MET survival receptor into a proapoptotic factor. ..
  3. Lindemann K, Resau J, Nahrig J, Kort E, Leeser B, Annecke K, et al. Differential expression of c-Met, its ligand HGF/SF and HER2/neu in DCIS and adjacent normal breast tissue. Histopathology. 2007;51:54-62 pubmed
    ..Moreover, c-Met and HGF/SF may contribute to tumour development by different means than those controlled by Her2/neu. ..
  4. Khor C, Grignani R, Ng D, Toh K, Chia K, Tan D, et al. cMET and refractive error progression in children. Ophthalmology. 2009;116:1469-74, 1474.e1 pubmed publisher
    ..To assess whether genetic variation in cMET is associated with refractive error or change in refractive error over time...
  5. Go H, Jeon Y, Park H, Sung S, Seo J, Chung D. High MET gene copy number leads to shorter survival in patients with non-small cell lung cancer. J Thorac Oncol. 2010;5:305-13 pubmed publisher
    ..019 and 0.008). Our results suggest that increased MET GCN would be an independent poor prognostic factor in SCC of the lung. ..
  6. Zhu G, Huang C, Qiu Z, Liu J, Zhang Z, Zhao N, et al. Expression and prognostic significance of CD151, c-Met, and integrin alpha3/alpha6 in pancreatic ductal adenocarcinoma. Dig Dis Sci. 2011;56:1090-8 pubmed publisher
    ..CD151, c-Met, and integrin alpha3/alpha6 were all overexpressed in PDAC. CD151 and c-Met might be new molecular markers to predict the prognosis of PDAC patients. ..
  7. Kim S, Lee U, Kim M, Lee E, Kim J, Lee M, et al. MicroRNA miR-199a* regulates the MET proto-oncogene and the downstream extracellular signal-regulated kinase 2 (ERK2). J Biol Chem. 2008;283:18158-66 pubmed publisher
    ..Coordinated down-regulation of both MET and its downstream effector ERK2 by miR-199a* may be effective in inhibiting not only cell proliferation but also motility and invasive capabilities of tumor cells. ..
  8. Migliore C, Petrelli A, Ghiso E, Corso S, Capparuccia L, Eramo A, et al. MicroRNAs impair MET-mediated invasive growth. Cancer Res. 2008;68:10128-36 pubmed publisher
    ..In conclusion, we have identified miRNAs that behave as oncosuppressors by negatively targeting MET and might thus provide an additional option to inhibit this oncogene in tumors displaying its deregulation. ..
  9. Gumustekin M, Kargi A, Bulut G, Gozukizil A, Ulukus C, Oztop I, et al. HGF/c-Met overexpressions, but not met mutation, correlates with progression of non-small cell lung cancer. Pathol Oncol Res. 2012;18:209-18 pubmed publisher
    ..The blockade of the HGF/c-Met pathway with RhoA and/or TIMP-3 inhibitors may be an effective therapeutic target for NSCLC treatment. ..
  10. Naldini L, Vigna E, Narsimhan R, Gaudino G, Zarnegar R, Michalopoulos G, et al. Hepatocyte growth factor (HGF) stimulates the tyrosine kinase activity of the receptor encoded by the proto-oncogene c-MET. Oncogene. 1991;6:501-4 pubmed
    ..These results suggest that HGF, or a growth factor structurally related to HGF, is a candidate ligand for the receptor encoded by c-MET. ..
  11. Schaeper U, Gehring N, Fuchs K, Sachs M, Kempkes B, Birchmeier W. Coupling of Gab1 to c-Met, Grb2, and Shp2 mediates biological responses. J Cell Biol. 2000;149:1419-32 pubmed
    ..Overexpression of a Gab1 mutant deficient in Shp2 interaction could also block HGF/SF-induced activation of the MAPK pathway, suggesting that Shp2 is critical for c-Met/Gab1-specific signaling. ..
  12. Ma P, Maulik G, Christensen J, Salgia R. c-Met: structure, functions and potential for therapeutic inhibition. Cancer Metastasis Rev. 2003;22:309-25 pubmed
    ..Most importantly, current data on c-Met suggest that when mutated or overexpressed in malignant cells, c-Met would serve as an important therapeutic target. ..
  13. Okuda K, Sasaki H, Yukiue H, Yano M, Fujii Y. Met gene copy number predicts the prognosis for completely resected non-small cell lung cancer. Cancer Sci. 2008;99:2280-5 pubmed publisher
    ..However, the results support a critical role of Met gene dose in NSCLC, suggesting that Met may be a specific molecular therapeutic target in selected NSCLC patients with increased Met copy number. ..
  14. Cappuzzo F, Marchetti A, Skokan M, Rossi E, Gajapathy S, Felicioni L, et al. Increased MET gene copy number negatively affects survival of surgically resected non-small-cell lung cancer patients. J Clin Oncol. 2009;27:1667-74 pubmed publisher
    ..66; P = .04). MET increased gene copy number is an independent negative prognostic factor in surgically resected NSCLC. EGFR gene gain does not impact survival after resection. ..
  15. Tremmel M, Matzke A, Albrecht I, Laib A, Olaku V, Ballmer Hofer K, et al. A CD44v6 peptide reveals a role of CD44 in VEGFR-2 signaling and angiogenesis. Blood. 2009;114:5236-44 pubmed publisher
  16. Yamamoto S, Tsuda H, Miyai K, Takano M, Tamai S, Matsubara O. Gene amplification and protein overexpression of MET are common events in ovarian clear-cell adenocarcinoma: their roles in tumor progression and prognostication of the patient. Mod Pathol. 2011;24:1146-55 pubmed publisher
    ..MET could serve as a biomarker for the prognostication of patients with clear-cell adenocarcinoma and tumor progression, and has potential as a novel therapeutic target for this carcinoma. ..
  17. Raghav K, Wang W, Liu S, Chavez MacGregor M, Meng X, Hortobagyi G, et al. cMET and phospho-cMET protein levels in breast cancers and survival outcomes. Clin Cancer Res. 2012;18:2269-77 pubmed publisher
    ..19-6.64, P = 0.019). High p-cMET level was associated with higher risk of recurrence (HR: 1.79, 95% CI: 1.08-2.95.77, P = 0.020). High levels of cMET and p-cMET were seen in all breast cancer subtypes and correlated with poor prognosis. ..
  18. Taher T, Tjin E, Beuling E, Borst J, Spaargaren M, Pals S. c-Cbl is involved in Met signaling in B cells and mediates hepatocyte growth factor-induced receptor ubiquitination. J Immunol. 2002;169:3793-800 pubmed
    ..Our findings identify c-Cbl as a negative regulator of HGF/Met signaling in B cells, mediating ubiquitination and, consequently, proteosomal degradation of Met, and suggest a role for Cbl in Met-mediated tumorigenesis. ..
  19. Gherardi E, Youles M, Miguel R, Blundell T, Iamele L, Gough J, et al. Functional map and domain structure of MET, the product of the c-met protooncogene and receptor for hepatocyte growth factor/scatter factor. Proc Natl Acad Sci U S A. 2003;100:12039-44 pubmed
    ..Our studies provide 3D models and a functional map of the MET ectodomain. They have broad implications for structure-function of the MET receptor and the related semaphorin and plexin proteins. ..
  20. Hashigasako A, Machide M, Nakamura T, Matsumoto K, Nakamura T. Bi-directional regulation of Ser-985 phosphorylation of c-met via protein kinase C and protein phosphatase 2A involves c-Met activation and cellular responsiveness to hepatocyte growth factor. J Biol Chem. 2004;279:26445-52 pubmed
  21. Kong Beltran M, Stamos J, Wickramasinghe D. The Sema domain of Met is necessary for receptor dimerization and activation. Cancer Cell. 2004;6:75-84 pubmed
    ..These data suggest that the Sema domain of Met may not only represent a novel anticancer therapeutic target but also acts as a biotherapeutic itself. ..
  22. Lutterbach B, Zeng Q, Davis L, Hatch H, Hang G, Kohl N, et al. Lung cancer cell lines harboring MET gene amplification are dependent on Met for growth and survival. Cancer Res. 2007;67:2081-8 pubmed
    ..These results strongly suggest that Met amplification identifies a subset of NSCLC likely to respond to new molecular therapies targeting Met. ..
  23. Campbell D, D Oronzio R, Garbett K, Ebert P, Mirnics K, Levitt P, et al. Disruption of cerebral cortex MET signaling in autism spectrum disorder. Ann Neurol. 2007;62:243-50 pubmed
    ..The complement of genes that encode proteins involved in MET activation appears to undergo long-term compensatory changes in expression that may be a hallmark contribution to the pathophysiology of ASD. ..
  24. Lee S, Kang S, Kim Y, Nam S, Lee D, Lee H, et al. [Expression of c-erbB-2 and c-met proteins in gastric adenoma and adenocarcinoma]. Korean J Gastroenterol. 2007;49:152-7 pubmed
    ..Although meaning for the expression of these proteins in gastric carcinomas would be different, these proteins may play as important oncogenes in gastric carcinogenesis. ..
  25. Seiden Long I, Navab R, Shih W, Li M, Chow J, Zhu C, et al. Gab1 but not Grb2 mediates tumor progression in Met overexpressing colorectal cancer cells. Carcinogenesis. 2008;29:647-55 pubmed publisher
    b>Hepatocyte growth factor receptor (Met) plays an important role in the progression of multiple cancer types...
  26. Turke A, Zejnullahu K, Wu Y, Song Y, Dias Santagata D, Lifshits E, et al. Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. Cancer Cell. 2010;17:77-88 pubmed publisher
    ..These findings highlight the potential to prospectively identify treatment naive, patients with EGFR-mutant lung cancer who will benefit from initial combination therapy. ..
  27. Benedettini E, Sholl L, Peyton M, Reilly J, Ware C, Davis L, et al. Met activation in non-small cell lung cancer is associated with de novo resistance to EGFR inhibitors and the development of brain metastasis. Am J Pathol. 2010;177:415-23 pubmed publisher
    ..If confirmed in larger cohorts, our analysis suggests that patient tumors harboring both Met activation and EGFR mutation could potentially benefit from early intervention with a combination of EGFR and Met inhibitors. ..
  28. Thanseem I, Nakamura K, Miyachi T, Toyota T, Yamada S, Tsujii M, et al. Further evidence for the role of MET in autism susceptibility. Neurosci Res. 2010;68:137-41 pubmed publisher
    ..4 kb. Our results provide further evidence for a possible role of MET in the pathogenesis of ASD. ..
  29. Hwang C, Matoso A, Corney D, Flesken Nikitin A, Körner S, Wang W, et al. Wild-type p53 controls cell motility and invasion by dual regulation of MET expression. Proc Natl Acad Sci U S A. 2011;108:14240-5 pubmed publisher
    ..These results also show that the extent of advanced cancer traits, such as invasion, may be determined by alterations in individual components of p53/MET regulatory network. ..
  30. Boccaccio C, Ando M, Tamagnone L, Bardelli A, Michieli P, Battistini C, et al. Induction of epithelial tubules by growth factor HGF depends on the STAT pathway. Nature. 1998;391:285-8 pubmed
    ..The HGF receptor tyrosine kinase works through a Src homology (SH2) docking site that can activate several signalling pathways...
  31. Giordano S, Corso S, Conrotto P, Artigiani S, Gilestro G, Barberis D, et al. The semaphorin 4D receptor controls invasive growth by coupling with Met. Nat Cell Biol. 2002;4:720-4 pubmed
    ..expressing the endogenous proteins, Plexin B1 (the Sema 4D Receptor) and Met (the Scatter Factor 1/ Hepatocyte Growth Factor Receptor) associate in a complex...
  32. Onozato R, Kosaka T, Kuwano H, Sekido Y, Yatabe Y, Mitsudomi T. Activation of MET by gene amplification or by splice mutations deleting the juxtamembrane domain in primary resected lung cancers. J Thorac Oncol. 2009;4:5-11 pubmed publisher
    ..About 5% of pulmonary adenocarcinomas in this cohort of Japanese patients were driven by activated MET by gene amplification or splice mutations. Such patients would be candidates for targeted therapy against MET. ..
  33. Cazet A, Bobowski M, Rombouts Y, Lefebvre J, Steenackers A, Popa I, et al. The ganglioside G(D2) induces the constitutive activation of c-Met in MDA-MB-231 breast cancer cells expressing the G(D3) synthase. Glycobiology. 2012;22:806-16 pubmed publisher
    ..The accumulation of G(D2) in c-Met expressing cells could therefore reinforce the tumorigenicity and aggressiveness of breast cancer tumors. ..
  34. Garouniatis A, Zizi Sermpetzoglou A, Rizos S, Kostakis A, Nikiteas N, Papavassiliou A. FAK, CD44v6, c-Met and EGFR in colorectal cancer parameters: tumour progression, metastasis, patient survival and receptor crosstalk. Int J Colorectal Dis. 2013;28:9-18 pubmed publisher
    ..Furthermore, we provide additional evidence for receptor interaction, properly clarifying their importance, which could potentially lead to more effective anti-CRC regimens. ..
  35. Trusolino L, Bertotti A, Comoglio P. A signaling adapter function for alpha6beta4 integrin in the control of HGF-dependent invasive growth. Cell. 2001;107:643-54 pubmed
    ..Such findings invoke an unexpected role for alpha6beta4 in cancer invasion as a functional amplifier of biochemical outputs rather than a mechanical adhesive device. ..
  36. Pozner Moulis S, Pappas D, Rimm D. Met, the hepatocyte growth factor receptor, localizes to the nucleus in cells at low density. Cancer Res. 2006;66:7976-82 pubmed
    ..This work suggests processing of the Met receptor, analogous to ErbB4, resulting in the release of the cytoplasmic domain and its translocation to the nucleus in cells at low density. ..
  37. Graziano F, Galluccio N, Lorenzini P, Ruzzo A, Canestrari E, D Emidio S, et al. Genetic activation of the MET pathway and prognosis of patients with high-risk, radically resected gastric cancer. J Clin Oncol. 2011;29:4789-95 pubmed publisher
    ..This marker was significantly associated with unfavorable prognosis. This information is relevant to the current clinical development of anti-MET compounds. ..
  38. Lee H, Kim M, Lee H, Jung E, Yang H, Lee B, et al. MET in gastric carcinomas: comparison between protein expression and gene copy number and impact on clinical outcome. Br J Cancer. 2012;107:325-33 pubmed publisher
    ..Also, the prognostic role of MET indicates that anti-MET therapy is a very promising modality in adjuvant treatment for gastric cancer. ..
  39. Li Y, Li A, Glas M, Lal B, Ying M, Sang Y, et al. c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype. Proc Natl Acad Sci U S A. 2011;108:9951-6 pubmed publisher
    ..These findings show that c-Met enhances the population of glioblastoma stem cells (GBM SCs) via a mechanism requiring Nanog and potentially other c-Met-responsive reprogramming transcription factors. ..
  40. Basilico C, Arnesano A, Galluzzo M, Comoglio P, Michieli P. A high affinity hepatocyte growth factor-binding site in the immunoglobulin-like region of Met. J Biol Chem. 2008;283:21267-77 pubmed publisher
    ..Although the IPT-HGF-alpha interaction provides binding strength, the Sema-HGF-beta contact confers selective sensitivity to the active form of the ligand. ..
  41. Yap T, Olmos D, Brunetto A, Tunariu N, Barriuso J, Riisnaes R, et al. Phase I trial of a selective c-MET inhibitor ARQ 197 incorporating proof of mechanism pharmacodynamic studies. J Clin Oncol. 2011;29:1271-9 pubmed publisher
    ..ARQ 197 safely inhibited intratumoral c-MET signaling. Further clinical evaluation focusing on combination approaches, including an erlotinib combination in non-small-cell lung cancer, is ongoing. ..
  42. Zhou X, Xu Y, Wang J, Zhou H, Liu X, Ayub Q, et al. Replication of the association of a MET variant with autism in a Chinese Han population. PLoS ONE. 2011;6:e27428 pubmed publisher
    ..This is the first attempt to replicate associations in Chinese autism samples, and our result provides evidence that MET variants may be relevant to autism susceptibility in the Chinese Han population. ..
  43. Gao J, Feng X, Inagaki Y, Song P, Kokudo N, Hasegawa K, et al. Des-?-carboxy prothrombin and c-Met were concurrently and extensively expressed in hepatocellular carcinoma and associated with tumor recurrence. Biosci Trends. 2012;6:153-9 pubmed
    ..Results of the current study suggested that DCP and c-Met are commonly and concurrently expressed in HCC and their absence is associated with a low risk of tumor recurrence. ..
  44. Maggiora P, Lorenzato A, Fracchioli S, Costa B, Castagnaro M, Arisio R, et al. The RON and MET oncogenes are co-expressed in human ovarian carcinomas and cooperate in activating invasiveness. Exp Cell Res. 2003;288:382-9 pubmed
    ..These data suggest that coexpression of the MET and RON receptors confer a selective advantage to ovarian cancer cells and might promote ovarian cancer progression. ..
  45. Niemann H, J ger V, Butler P, van den Heuvel J, Schmidt S, Ferraris D, et al. Structure of the human receptor tyrosine kinase met in complex with the Listeria invasion protein InlB. Cell. 2007;130:235-46 pubmed publisher
    ..Thus, although it elicits a similar cellular response, InlB is not a structural mimic of HGF/SF...
  46. Ghadjar P, Blank Liss W, Simcock M, Hegyi I, Beer K, Moch H, et al. MET Y1253D-activating point mutation and development of distant metastasis in advanced head and neck cancers. Clin Exp Metastasis. 2009;26:809-15 pubmed publisher
    ..1, 5.8). The observed association between MET Y1253D-activating point mutation and decreased distant metastasis-free survival in advanced HNSCC suggests that MET may be a potential target for specific treatment interventions. ..
  47. Herrera L, El Hefnawy T, Queiroz de Oliveira P, Raja S, Finkelstein S, Gooding W, et al. The HGF receptor c-Met is overexpressed in esophageal adenocarcinoma. Neoplasia. 2005;7:75-84 pubmed
    ..Met dysregulation occurs early in Barrett's dysplasia to adenocarcinoma sequence. Future study of Met inhibition as a potential biologic therapy for EA is warranted. ..
  48. Petrelli A, Gilestro G, Lanzardo S, Comoglio P, Migone N, Giordano S. The endophilin-CIN85-Cbl complex mediates ligand-dependent downregulation of c-Met. Nature. 2002;416:187-90 pubmed
    ..growth factor (HGF) receptor (Met) is polyubiquitinated and degraded; however, the mechanisms underlying HGF receptor endocytosis are not yet known...
  49. Campbell D, Buie T, Winter H, Bauman M, Sutcliffe J, Perrin J, et al. Distinct genetic risk based on association of MET in families with co-occurring autism and gastrointestinal conditions. Pediatrics. 2009;123:1018-24 pubmed publisher
    ..These results suggest that disrupted MET signaling may contribute to increased risk for autism spectrum disorder that includes familial gastrointestinal dysfunction. ..
  50. Gherardi E, Sandin S, Petoukhov M, Finch J, Youles M, Ofverstedt L, et al. Structural basis of hepatocyte growth factor/scatter factor and MET signalling. Proc Natl Acad Sci U S A. 2006;103:4046-51 pubmed
  51. Janjigian Y, Tang L, Coit D, Kelsen D, Francone T, Weiser M, et al. MET expression and amplification in patients with localized gastric cancer. Cancer Epidemiol Biomarkers Prev. 2011;20:1021-7 pubmed publisher
    ..This article shows a lack of MET amplification and pathway activation in a cohort of 38 patients with localized gastric cancer, suggesting that MET-driven gastric cancers are relatively rare in Western patients. ..
  52. Artigiani S, Conrotto P, Fazzari P, Gilestro G, Barberis D, Giordano S, et al. Plexin-B3 is a functional receptor for semaphorin 5A. EMBO Rep. 2004;5:710-4 pubmed
    ..In addition, Sema5A can trigger the intracellular signalling of the hepatocyte growth factor/scatter factor receptor, Met, associated in a complex with plexin-B3...
  53. Conrotto P, Valdembri D, Corso S, Serini G, Tamagnone L, Comoglio P, et al. Sema4D induces angiogenesis through Met recruitment by Plexin B1. Blood. 2005;105:4321-9 pubmed
    ..In sum, we identify a proangiogenic semaphorin and provide insight about the signaling machinery exploited by Plexin B1 to control angiogenesis. ..
  54. van Leenders G, Sookhlall R, Teubel W, de Ridder C, Reneman S, Sacchetti A, et al. Activation of c-MET induces a stem-like phenotype in human prostate cancer. PLoS ONE. 2011;6:e26753 pubmed publisher
    ..Its mediation of efficient tumour-formation in vivo and predominant receptor expression at the invasive front implicate that c-MET regulates tumour infiltration in surrounding tissues putatively by acquisition of a stem-like phenotype. ..
  55. Kanteti R, Nallasura V, Loganathan S, Tretiakova M, Kroll T, Krishnaswamy S, et al. PAX5 is expressed in small-cell lung cancer and positively regulates c-Met transcription. Lab Invest. 2009;89:301-14 pubmed publisher
    ..Therefore, we propose that PAX5 could be an important regulator of c-Met transcription and a potential target for therapy in SCLC. ..
  56. Tsuta K, Kozu Y, Mimae T, Yoshida A, Kohno T, Sekine I, et al. c-MET/phospho-MET protein expression and MET gene copy number in non-small cell lung carcinomas. J Thorac Oncol. 2012;7:331-9 pubmed publisher
    ..Among ADCs, c-MET expression and MET BISH positivity were more common in poorly differentiated cases. MET BISH positivity was an independent prognostic factor in nonsquamous NSCLCs. ..
  57. Matteucci E, Bendinelli P, Desiderio M. Nuclear localization of active HGF receptor Met in aggressive MDA-MB231 breast carcinoma cells. Carcinogenesis. 2009;30:937-45 pubmed publisher
    ..Wwox/Met system can be suggested as a potential target to impair breast carcinoma progression. ..
  58. Ostroumov E, Hunter C. Identifying mechanisms for therapeutic intervention in chordoma: c-Met oncoprotein. Spine (Phila Pa 1976). 2008;33:2774-80 pubmed publisher
    ..A human sacral chordoma cell line, CCL3, was established and in vitro characterization of c-Met oncoprotein in chordoma cells was performed...
  59. Burdick K, DeRosse P, Kane J, Lencz T, Malhotra A. Association of genetic variation in the MET proto-oncogene with schizophrenia and general cognitive ability. Am J Psychiatry. 2010;167:436-43 pubmed publisher
    ..These results add to the growing evidence suggesting an intriguing relationship between cancer-related genes and schizophrenia susceptibility. ..
  60. Tulasne D, Paumelle R, Weidner K, Vandenbunder B, Fafeur V. The multisubstrate docking site of the MET receptor is dispensable for MET-mediated RAS signaling and cell scattering. Mol Biol Cell. 1999;10:551-65 pubmed
    ..We propose that signal transduction by autophosphorylation of the C-terminal tyrosine residues is not the sole mechanism by which the activated MET receptor can transmit RAS signaling and cell scattering. ..
  61. Jo M, Stolz D, Esplen J, Dorko K, Michalopoulos G, Strom S. Cross-talk between epidermal growth factor receptor and c-Met signal pathways in transformed cells. J Biol Chem. 2000;275:8806-11 pubmed
    ..This cross-talk between c-Met and EGFR may have significant implications for altered growth control in tumorigenesis. ..
  62. Crostella L, Lidder S, Williams R, Skouteris G. Hepatocyte Growth Factor/scatter factor-induces phosphorylation of cortactin in A431 cells in a Src kinase-independent manner. Oncogene. 2001;20:3735-45 pubmed
    The Hepatocyte Growth Factor receptor transduces proliferating and scattering signals in epithelial and endothelial cells...
  63. Stella M, Trusolino L, Pennacchietti S, Comoglio P. Negative feedback regulation of Met-dependent invasive growth by Notch. Mol Cell Biol. 2005;25:3982-96 pubmed
    ..These results unravel an in-built mechanism of negative feedback regulation in which Met activation leads to transcriptional induction of Notch function, which in turn limits HGF activity through repression of the Met oncogene. ..
  64. Kirchhofer D, Lipari M, Santell L, Billeci K, Maun H, Sandoval W, et al. Utilizing the activation mechanism of serine proteases to engineer hepatocyte growth factor into a Met antagonist. Proc Natl Acad Sci U S A. 2007;104:5306-11 pubmed
    ..Thus, although serine proteases and HGF have quite distinct functions in proteolysis and Met signal transduction, respectively, they share a similar activation mechanism. ..
  65. Onitsuka T, Uramoto H, Ono K, Takenoyama M, Hanagiri T, Oyama T, et al. Comprehensive molecular analyses of lung adenocarcinoma with regard to the epidermal growth factor receptor, K-ras, MET, and hepatocyte growth factor status. J Thorac Oncol. 2010;5:591-6 pubmed publisher
    ..The wild type of K-ras, negative p-MET 1234/1235, and positive expression of HGF may be a useful marker for predicting poor prognosis of patients who underwent surgical resection of lung adenocarcinoma. ..
  66. Gual P, Giordano S, Williams T, Rocchi S, Van Obberghen E, Comoglio P. Sustained recruitment of phospholipase C-gamma to Gab1 is required for HGF-induced branching tubulogenesis. Oncogene. 2000;19:1509-18 pubmed
    ..The HGF receptor directly activates PI3 kinase, Ras and STAT signalling pathways and phosphorylates the adaptator GRB2 ..
  67. Athauda G, Giubellino A, Coleman J, Horak C, Steeg P, Lee M, et al. c-Met ectodomain shedding rate correlates with malignant potential. Clin Cancer Res. 2006;12:4154-62 pubmed
    ..92, linear regression). For a variety of human cancers, c-Met ectodomain shedding may provide a reliable and practical indicator of malignant potential and overall tumor burden. ..
  68. Cappuzzo F, Jänne P, Skokan M, Finocchiaro G, Rossi E, Ligorio C, et al. MET increased gene copy number and primary resistance to gefitinib therapy in non-small-cell lung cancer patients. Ann Oncol. 2009;20:298-304 pubmed publisher
    ..MET gene amplification is a rare event in patients with advanced NSCLC. The development of anti-MET therapeutic strategies should be focused on patients with acquired EGFR-TKI resistance. ..
  69. Gao X, Lorinczi M, Hill K, Brooks N, Dokainish H, Ireton K, et al. Met receptor tyrosine kinase degradation is altered in response to the leucine-rich repeat of the Listeria invasion protein internalin B. J Biol Chem. 2009;284:774-83 pubmed publisher
    ..involves binding of the bacterial protein Internalin B to the host receptor tyrosine kinase Met (hepatocyte growth factor receptor). Activation of Met and downstream signaling cascades is critical for Listeria entry...
  70. Graveel C, DeGroot J, Su Y, Koeman J, Dykema K, Leung S, et al. Met induces diverse mammary carcinomas in mice and is associated with human basal breast cancer. Proc Natl Acad Sci U S A. 2009;106:12909-14 pubmed publisher
    ..We conclude from these studies that MET may play a critical role in the development of the most aggressive breast cancers and may be a rational therapeutic target...
  71. Monga S, Mars W, Pediaditakis P, Bell A, Mulè K, Bowen W, et al. Hepatocyte growth factor induces Wnt-independent nuclear translocation of beta-catenin after Met-beta-catenin dissociation in hepatocytes. Cancer Res. 2002;62:2064-71 pubmed
    ..Part of the multifunctionality of HGF might be attributable to nuclear beta-catenin and the resulting target gene expression. ..
  72. Campbell D, Sutcliffe J, Ebert P, Militerni R, Bravaccio C, Trillo S, et al. A genetic variant that disrupts MET transcription is associated with autism. Proc Natl Acad Sci U S A. 2006;103:16834-9 pubmed
    ..These data implicate reduced MET gene expression in autism susceptibility, providing evidence of a previously undescribed pathophysiological basis for this behaviorally and medically complex disorder. ..
  73. Yanovitch T, Li Y, Metlapally R, Abbott D, Viet K, Young T. Hepatocyte growth factor and myopia: genetic association analyses in a Caucasian population. Mol Vis. 2009;15:1028-35 pubmed
    Hepatocyte growth factor (HGF) and hepatocyte growth factor receptor (C-MET) genes have previously been reported to be associated with myopia in Asian family-based and case-control association studies, respectively...
  74. Han C, Ma J, Li F, Zhao J, Jing W, Zhou Y, et al. EGFR and KRAS mutations and altered c-Met gene copy numbers in primary non-small cell lung cancer and associated stage N2 lymph node-metastasis. Cancer Lett. 2012;314:63-72 pubmed publisher
    ..c-Met GCN was increased significantly in EGFR TKI-naive patients with lymph node-metastatic tumors. ..
  75. Mineo R, Costantino A, Frasca F, Sciacca L, Russo S, Vigneri R, et al. Activation of the hepatocyte growth factor (HGF)-Met system in papillary thyroid cancer: biological effects of HGF in thyroid cancer cells depend on Met expression levels. Endocrinology. 2004;145:4355-65 pubmed
  76. Grabellus F, Konik M, Worm K, Sheu S, van de Nes J, Bauer S, et al. MET overexpressing chordomas frequently exhibit polysomy of chromosome 7 but no MET activation through sarcoma-specific gene fusions. Tumour Biol. 2010;31:157-63 pubmed publisher
    ..A clear influence of polysomy 7 on MET protein expression could not be statistically demonstrated for this cohort. Moreover, gene fusions with the ability to cause MET overexpression do not occur in chordomas. ..
  77. Liu Y, Li Q, Zhu L. Expression of the hepatocyte growth factor and c-Met in colon cancer: correlation with clinicopathological features and overall survival. Tumori. 2012;98:105-12 pubmed publisher
    ..In the study, we analyzed the expression of HGF and c-Met in colon cancer and assessed the influence of the expression of this growth factor and its receptor on clinical and histological parameters and patient survival...
  78. Cassinelli G, Favini E, Degl Innocenti D, Salvi A, De Petro G, Pierotti M, et al. RET/PTC1-driven neoplastic transformation and proinvasive phenotype of human thyrocytes involve Met induction and beta-catenin nuclear translocation. Neoplasia. 2009;11:10-21 pubmed
    ..Such molecular network, promoting disease initiation and acquisition of a proinvasive phenotype, highlights new options to design multitarget therapeutic strategies for PTCs. ..
  79. Rickert K, Patel S, Allison T, Byrne N, Darke P, Ford R, et al. Structural basis for selective small molecule kinase inhibition of activated c-Met. J Biol Chem. 2011;286:11218-25 pubmed publisher
    ..The results highlight the role of structural plasticity within the kinase domain in imparting the specificity of ligand binding and provide the framework for structure-guided design of activated c-Met inhibitors. ..
  80. Bottaro D, Rubin J, Faletto D, Chan A, Kmiecik T, Vande Woude G, et al. Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product. Science. 1991;251:802-4 pubmed
    ..Covalent cross-linking of 125I-labeled ligand to cellular proteins of appropriate size that were recognized by antibodies to c-met directly established the c-met product as the cell-surface receptor for HGF. ..
  81. Bean J, Brennan C, Shih J, Riely G, Viale A, Wang L, et al. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A. 2007;104:20932-7 pubmed
    ..Taken together, these data suggest that MET amplification occurs independently of EGFR(T790M) mutations and that MET may be a clinically relevant therapeutic target for some patients with acquired resistance to gefitinib or erlotinib. ..
  82. Zeng Z, Weiser M, Kuntz E, Chen C, Khan S, Forslund A, et al. c-Met gene amplification is associated with advanced stage colorectal cancer and liver metastases. Cancer Lett. 2008;265:258-69 pubmed publisher
    ..c-Met gene amplification is linked to metastatic progression, and is a viable target for a significant subset of advanced CRC. ..
  83. Eathiraj S, Palma R, Volckova E, Hirschi M, France D, Ashwell M, et al. Discovery of a novel mode of protein kinase inhibition characterized by the mechanism of inhibition of human mesenchymal-epithelial transition factor (c-Met) protein autophosphorylation by ARQ 197. J Biol Chem. 2011;286:20666-76 pubmed publisher
  84. Previdi S, Abbadessa G, Dalò F, France D, Broggini M. Breast cancer-derived bone metastasis can be effectively reduced through specific c-MET inhibitor tivantinib (ARQ 197) and shRNA c-MET knockdown. Mol Cancer Ther. 2012;11:214-23 pubmed publisher
  85. Kondo S, Ojima H, Tsuda H, Hashimoto J, Morizane C, Ikeda M, et al. Clinical impact of c-Met expression and its gene amplification in hepatocellular carcinoma. Int J Clin Oncol. 2013;18:207-13 pubmed publisher
    ..Although c-Met expression was not significantly associated with c-Met gene amplification, it may be a useful predictive marker of recurrence in resected HCC patients. ..
  86. van Leenders G, van Balken B, Aalders T, Hulsbergen van de Kaa C, Ruiter D, Schalken J. Intermediate cells in normal and malignant prostate epithelium express c-MET: implications for prostate cancer invasion. Prostate. 2002;51:98-107 pubmed
    ..6 +/- 2.4 mm(2) in controls (P < 0.02). Intermediate cells in normal and malignant prostate epithelium express high c-MET levels, indicating that they are prone to stromal invasion in prostate carcinoma. ..
  87. Guo A, Villen J, Kornhauser J, Lee K, Stokes M, Rikova K, et al. Signaling networks assembled by oncogenic EGFR and c-Met. Proc Natl Acad Sci U S A. 2008;105:692-7 pubmed publisher
    ..Comparison of the signaling networks in EGFR and c-Met-dependent cells identify a "core network" of approximately 50 proteins that participate in pathways mediating drug response. ..
  88. Foveau B, Ancot F, Leroy C, Petrelli A, Reiss K, Vingtdeux V, et al. Down-regulation of the met receptor tyrosine kinase by presenilin-dependent regulated intramembrane proteolysis. Mol Biol Cell. 2009;20:2495-507 pubmed publisher
    ..This demonstrates the original involvement of a proteolytic process in degradation of the Met receptor implicated in negative regulation of invasive growth. ..
  89. Lee J, Seo J, Jun H, Ki C, Park S, Park Y, et al. Impact of MET amplification on gastric cancer: possible roles as a novel prognostic marker and a potential therapeutic target. Oncol Rep. 2011;25:1517-24 pubmed publisher
    ..However, the predictive role of MET amplification for treatment response should be further explored in upcoming clinical trials. ..
  90. Acunzo M, Visone R, Romano G, Veronese A, Lovat F, Palmieri D, et al. miR-130a targets MET and induces TRAIL-sensitivity in NSCLC by downregulating miR-221 and 222. Oncogene. 2012;31:634-42 pubmed publisher
    ..Moreover, we found that miR-130a reduced migratory capacity of NSCLC. A better understanding of MET-miR-221 and 222 axis regulation in drug resistance is the key in developing new strategies in NSCLC therapy. ..
  91. Park S, Choi Y, Sung C, An J, Seo J, Ahn M, et al. High MET copy number and MET overexpression: poor outcome in non-small cell lung cancer patients. Histol Histopathol. 2012;27:197-207 pubmed publisher
    ..618; 95% confidence interval, 1.066-2.456; p=0.024). Increased MET copy number and MET overexpression are negative prognostic factors for surgically resected NSCLCs. ..
  92. Weidner K, Sachs M, Riethmacher D, Birchmeier W. Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells. Proc Natl Acad Sci U S A. 1995;92:2597-601 pubmed
    ..The opposite roles of the juxtamembrane and C-terminal tyrosine residues may explain the suggested dual function of the met receptor in both epithelial-mesenchymal interactions and tumor progression. ..