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

Publications192 found, 100 shown here

  1. Lu K, Chang J, Parachoniak C, Pandika M, Aghi M, Meyronet D, et al. VEGF inhibits tumor cell invasion and mesenchymal transition through a MET/VEGFR2 complex. Cancer Cell. 2012;22:21-35 pubmed publisher
    ..Inhibition of MET in GBM mouse models blocks mesenchymal transition and invasion provoked by VEGF ablation, resulting in substantial survival benefit. ..
  2. Park W, Dong S, Kim S, Na E, Shin M, Pi J, et al. Somatic mutations in the kinase domain of the Met/hepatocyte growth factor receptor gene in childhood hepatocellular carcinomas. Cancer Res. 1999;59:307-10 pubmed
    ..Our results indicate that mutations of the tyrosine kinase domain of the MET gene may be involved in the acceleration of the carcinogenesis in childhood HCC. ..
  3. Krishnaswamy S, Kanteti R, Duke Cohan J, Loganathan S, Liu W, Ma P, et al. Ethnic differences and functional analysis of MET mutations in lung cancer. Clin Cancer Res. 2009;15:5714-23 pubmed publisher
    ..All the MET mutations were germline. East Asians, African-Americans, and Caucasians had different MET genotypes and haplotypes. MET mutations in the semaphorin domain affected ligand binding. ..
  4. Catenacci D, Henderson L, Xiao S, Patel P, Yauch R, Hegde P, et al. Durable complete response of metastatic gastric cancer with anti-Met therapy followed by resistance at recurrence. Cancer Discov. 2011;1:573-9 pubmed publisher
    ..It is also the first to report biomarkers that predicted therapeutic response to Met inhibition. ..
  5. Sangwan V, Paliouras G, Abella J, Dubé N, Monast A, Tremblay M, et al. Regulation of the Met receptor-tyrosine kinase by the protein-tyrosine phosphatase 1B and T-cell phosphatase. J Biol Chem. 2008;283:34374-83 pubmed publisher
    ..We have identified PTP1B and TCPTP as negative regulators of the hepatocyte growth factor receptor, the Met receptor-tyrosine kinase...
  6. Derksen P, de Gorter D, Meijer H, Bende R, van Dijk M, Lokhorst H, et al. The hepatocyte growth factor/Met pathway controls proliferation and apoptosis in multiple myeloma. Leukemia. 2003;17:764-74 pubmed
    ..Taken together, our data indicate that HGF is a potent myeloma growth and survival factor and suggest that the HGF/Met pathway is a potential therapeutic target in MM. ..
  7. Walter B, Begnami M, Valera V, Santi M, Rushing E, Quezado M. Gain of chromosome 7 by chromogenic in situ hybridization (CISH) in chordomas is correlated to c-MET expression. J Neurooncol. 2011;101:199-206 pubmed publisher
    ..c-MET overexpression shows promise as a molecular marker of response to targeted molecular therapy in the treatment of chordomas...
  8. Minuti G, Cappuzzo F, Duchnowska R, Jassem J, Fabi A, O BRIEN T, et al. Increased MET and HGF gene copy numbers are associated with trastuzumab failure in HER2-positive metastatic breast cancer. Br J Cancer. 2012;107:793-9 pubmed publisher
    ..001) and combination of both biomarkers did not increase predictive value of either considered separately. High GCNs of MET and HGF associate with an increased risk of trastuzumab-based therapy failure in HER2-positive MBC. ..
  9. Lock L, Frigault M, Saucier C, Park M. Grb2-independent recruitment of Gab1 requires the C-terminal lobe and structural integrity of the Met receptor kinase domain. J Biol Chem. 2003;278:30083-90 pubmed
    ..In addition, Gab1 interacts with the Met/hepatocyte growth factor receptor in a Grb2-independent manner...
  10. Singleton P, Salgia R, Moreno Vinasco L, Moitra J, Sammani S, Mirzapoiazova T, et al. CD44 regulates hepatocyte growth factor-mediated vascular integrity. Role of c-Met, Tiam1/Rac1, dynamin 2, and cortactin. J Biol Chem. 2007;282:30643-57 pubmed
    ..Taken together, these results suggest that CD44 is an important regulator of HGF/c-Met-mediated in vitro and in vivo barrier enhancement, a process with essential involvement of Tiam1, Rac1, dynamin 2, and cortactin. ..
  11. Swiercz J, Worzfeld T, Offermanns S. ErbB-2 and met reciprocally regulate cellular signaling via plexin-B1. J Biol Chem. 2008;283:1893-901 pubmed
    ..This work identifies a novel mechanism by which plexin-mediated signaling can be regulated and explains how Sema4D can exert different biological activities through the differential association of its receptor with ErbB-2 and Met. ..
  12. Stellrecht C, Gandhi V. MET receptor tyrosine kinase as a therapeutic anticancer target. Cancer Lett. 2009;280:1-14 pubmed publisher
    ..Numerous agents have been developed that are able to target MET expression and/or function and are the focus of this review. ..
  13. Tachibana K, Minami Y, Shiba Ishii A, Kano J, Nakazato Y, Sato Y, et al. Abnormality of the hepatocyte growth factor/MET pathway in pulmonary adenocarcinogenesis. Lung Cancer. 2012;75:181-8 pubmed publisher
    ..An increased MET gene copy number is indicative of a poor outcome in patients with small pulmonary adenocarcinomas. ..
  14. Park M, Dean M, Kaul K, Braun M, Gonda M, Vande Woude G. Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors. Proc Natl Acad Sci U S A. 1987;84:6379-83 pubmed
    ..We conclude from these results that the MET protooncogene is a cell-surface receptor for an as-yet-unknown ligand. ..
  15. Row P, Clague M, Urbé S. Growth factors induce differential phosphorylation profiles of the Hrs-STAM complex: a common node in signalling networks with signal-specific properties. Biochem J. 2005;389:629-36 pubmed
  16. Miyata Y, Sagara Y, Kanda S, Hayashi T, Kanetake H. Phosphorylated hepatocyte growth factor receptor/c-Met is associated with tumor growth and prognosis in patients with bladder cancer: correlation with matrix metalloproteinase-2 and -7 and E-cadherin. Hum Pathol. 2009;40:496-504 pubmed publisher
    b>Hepatocyte growth factor receptor/c-Met is associated with malignant aggressiveness and survival in various cancers including bladder cancer...
  17. Campbell D, Warren D, Sutcliffe J, Lee E, Levitt P. Association of MET with social and communication phenotypes in individuals with autism spectrum disorder. Am J Med Genet B Neuropsychiatr Genet. 2010;153B:438-446 pubmed publisher
    ..These data indicate that the MET C allele influences at least two of the three domains of the autism triad. ..
  18. Jackson P, Boccuto L, Skinner C, Collins J, Neri G, Gurrieri F, et al. Further evidence that the rs1858830 C variant in the promoter region of the MET gene is associated with autistic disorder. Autism Res. 2009;2:232-6 pubmed publisher
    ..20; 95% CI=0.56-2.56; chi(2)=0.2, df=1, P=0.64). This study is the third independent study to find the rs1858830 C variant in the MET gene promoter to be associated with autism. ..
  19. Chen Y, Chang J, Liu H, Yu T, Chiu Y, Hsieh J, et al. Clinical implications of high MET gene dosage in non-small cell lung cancer patients without previous tyrosine kinase inhibitor treatment. J Thorac Oncol. 2011;6:2027-35 pubmed publisher
    ..042) by univariate analysis. High MET gene dosage was not related to primary TKI resistance and the incidence was increased after chemotherapy, suggesting high MET gene dosage may also be related to chemotherapy resistance. ..
  20. Dean M, Park M, Le Beau M, Robins T, Diaz M, Rowley J, et al. The human met oncogene is related to the tyrosine kinase oncogenes. Nature. 1985;318:385-8 pubmed
    ..The accompanying paper shows that this chromosomal locus is also tightly linked with the human heredity disease cystic fibrosis. ..
  21. Deheuninck J, Goormachtigh G, Foveau B, Ji Z, Leroy C, Ancot F, et al. Phosphorylation of the MET receptor on juxtamembrane tyrosine residue 1001 inhibits its caspase-dependent cleavage. Cell Signal. 2009;21:1455-63 pubmed publisher
    ..These data demonstrate a direct protection mechanism of an activated phosphorylated MET receptor, against its caspase-dependent cleavage. ..
  22. Liu X, Wang Q, Yang G, Marando C, Koblish H, Hall L, et al. A novel kinase inhibitor, INCB28060, blocks c-MET-dependent signaling, neoplastic activities, and cross-talk with EGFR and HER-3. Clin Cancer Res. 2011;17:7127-38 pubmed publisher
    ..INCB28060 is a potent and selective c-MET kinase inhibitor that may have therapeutic potential in cancer treatment. ..
  23. De Bacco F, Casanova E, Medico E, Pellegatta S, Orzan F, Albano R, et al. The MET oncogene is a functional marker of a glioblastoma stem cell subtype. Cancer Res. 2012;72:4537-50 pubmed publisher
    ..Together, our findings suggest that Met is a functional marker of glioblastoma stem cells and a candidate target for identification and therapy of a subset of glioblastomas. ..
  24. Gibney G, Aziz S, Camp R, Conrad P, Schwartz B, Chen C, et al. c-Met is a prognostic marker and potential therapeutic target in clear cell renal cell carcinoma. Ann Oncol. 2013;24:343-9 pubmed publisher
    ..c-Met is associated with poor pathologic features and prognosis in RCC. c-Met inhibition demonstrates in vitro activity against clear cell RCC. Further study of ARQ 197 with appropriate biomarker studies in RCC is warranted. ..
  25. 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. ..
  26. 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. ..
  27. 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. ..
  28. 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...
  29. 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. ..
  30. 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. ..
  31. 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. ..
  32. 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. ..
  33. 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. ..
  34. 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. ..
  35. 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. ..
  36. 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. ..
  37. 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. ..
  38. 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. ..
  39. 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
  40. 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. ..
  41. 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. ..
  42. 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. ..
  43. 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. ..
  44. 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
  45. 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. ..
  46. 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. ..
  47. 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. ..
  48. 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. ..
  49. 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...
  50. 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. ..
  51. 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. ..
  52. 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. ..
  53. 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. ..
  54. 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...
  55. 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...
  56. 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. ..
  57. 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. ..
  58. 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. ..
  59. 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. ..
  60. 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. ..
  61. 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. ..
  62. 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. ..
  63. 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. ..
  64. 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. ..
  65. 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. ..
  66. 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. ..
  67. 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. ..
  68. 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. ..
  69. 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...
  70. 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. ..
  71. 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. ..
  72. 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...
  73. 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. ..
  74. 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
  75. 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. ..
  76. 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...
  77. 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. ..
  78. 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. ..
  79. 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. ..
  80. 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. ..
  81. 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. ..
  82. 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...
  83. 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. ..
  84. 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. ..
  85. 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. ..
  86. 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...
  87. 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. ..
  88. 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. ..
  89. 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. ..
  90. 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 ..