contact inhibition

Summary

Summary: Arrest of cell locomotion or cell division when two cells come into contact.

Top Publications

  1. Carmona Fontaine C, Matthews H, Kuriyama S, Moreno M, Dunn G, Parsons M, et al. Contact inhibition of locomotion in vivo controls neural crest directional migration. Nature. 2008;456:957-61 pubmed publisher
    b>Contact inhibition of locomotion was discovered by Abercrombie more than 50 years ago and describes the behaviour of fibroblast cells confronting each other in vitro, where they retract their protrusions and change direction on contact...
  2. Puliafito A, Hufnagel L, Neveu P, Streichan S, Sigal A, Fygenson D, et al. Collective and single cell behavior in epithelial contact inhibition. Proc Natl Acad Sci U S A. 2012;109:739-44 pubmed publisher
    ..is encountered in vitro in normally differentiating epithelial cell cultures and is known as "contact inhibition." The study presented here provides a quantitative characterization of contact inhibition dynamics on ..
  3. Ose R, Yanagawa T, Ikeda S, Ohara O, Koga H. PCDH24-induced contact inhibition involves downregulation of beta-catenin signaling. Mol Oncol. 2009;3:54-66 pubmed publisher
    ..Elevated expression of the protocadherin LKC (PCDH24) in HCT116 colon carcinoma cells has been shown to induce contact inhibition, thereby completely abolishing tumor formation in vivo (Carcinogenesis, 2002; 23(7):1139-1148)...
  4. Lu L, Teixeira V, Yuan Z, Graham T, Endesfelder D, Kolluri K, et al. LRIG1 regulates cadherin-dependent contact inhibition directing epithelial homeostasis and pre-invasive squamous cell carcinoma development. J Pathol. 2013;229:608-20 pubmed publisher
    ..We show that deletion of Lrig1 is sufficient to promote murine airway hyperplasia through loss of contact inhibition and that re-expression of LRIG1 in human lung cancer cells inhibits tumourigenesis...
  5. Joyce N, Harris D, Mello D. Mechanisms of mitotic inhibition in corneal endothelium: contact inhibition and TGF-beta2. Invest Ophthalmol Vis Sci. 2002;43:2152-9 pubmed
    b>Contact inhibition has been implicated as an important antiproliferative mechanism in developing and mature corneal endothelium...
  6. Okada T, Lopez Lago M, Giancotti F. Merlin/NF-2 mediates contact inhibition of growth by suppressing recruitment of Rac to the plasma membrane. J Cell Biol. 2005;171:361-71 pubmed
    Introduction of activated p21-activated kinase (PAK) is sufficient to release primary endothelial cells from contact inhibition of growth...
  7. Vinals F, Pouyssegur J. Confluence of vascular endothelial cells induces cell cycle exit by inhibiting p42/p44 mitogen-activated protein kinase activity. Mol Cell Biol. 1999;19:2763-72 pubmed
    ..Therefore, inhibition of p42/p44 MAPK activation by cell-cell contact is a critical step initiating cell cycle exit in vascular endothelial cells. ..
  8. Kim J, Asthagiri A. Matrix stiffening sensitizes epithelial cells to EGF and enables the loss of contact inhibition of proliferation. J Cell Sci. 2011;124:1280-7 pubmed publisher
    ..stiffening of the matrix reduces the threshold amount of epidermal growth factor (EGF) needed to over-ride contact inhibition by over 100-fold...
  9. Shumate S, El Shenawee M. Computational model of ductal carcinoma in situ: the effects of contact inhibition on pattern formation. IEEE Trans Biomed Eng. 2009;56:1341-7 pubmed publisher
    ..automaton model based on observed phenotypic characteristics of DCIS emphasize the important role of contact inhibition on lesion pattern formation...

More Information

Publications62

  1. Slisz M, Rothenberger E, Hutter D. Attenuation of p38 MAPK activity upon contact inhibition in fibroblasts. Mol Cell Biochem. 2008;308:65-73 pubmed
    The molecular events, which govern growth control upon contact inhibition have not yet been clearly defined...
  2. Baba T, Kariya M, Higuchi T, Mandai M, Matsumura N, Kondoh E, et al. Neuropilin-1 promotes unlimited growth of ovarian cancer by evading contact inhibition. Gynecol Oncol. 2007;105:703-11 pubmed
    ..that persistently high expression of NRP-1 in ovarian cancer enhances proliferation through evasion of contact inhibition. Suppression of NRP-1 also decreased cell growth in soft agar and invasion to the extracellular matrix in ..
  3. Vutskits G, Salmon P, Mayor L, Vutskits L, Cudré Mauroux C, Soriano J, et al. A role for atm in E-cadherin-mediated contact inhibition in epithelial cells. Breast Cancer Res Treat. 2006;99:143-53 pubmed
    ..Here, we propose a novel role for atm in cultured epithelial cells, namely the regulation of cell growth by contact inhibition. We show that atm is upregulated in epithelial cells reaching confluence...
  4. Tanaka M, Kuriyama S, Aiba N. Nm23-H1 regulates contact inhibition of locomotion, which is affected by ephrin-B1. J Cell Sci. 2012;125:4343-53 pubmed publisher
    b>Contact inhibition of locomotion (CIL) is the process by which cells stop the continual migration in the same direction after collision with another cell...
  5. Regl G, Kasper M, Schnidar H, Eichberger T, Neill G, Ikram M, et al. The zinc-finger transcription factor GLI2 antagonizes contact inhibition and differentiation of human epidermal cells. Oncogene. 2004;23:1263-74 pubmed
    ..Here, we provide evidence for a role of human GLI2 in antagonizing contact inhibition and epidermal differentiation...
  6. Vizirianakis I, Chen Y, Kantak S, Tsiftsoglou A, Kramer R. Dominant-negative E-cadherin alters adhesion and reverses contact inhibition of growth in breast carcinoma cells. Int J Oncol. 2002;21:135-44 pubmed
    ..Overall, these observations suggest that in breast carcinoma, disruption of E-cadherin and catenin function modulates both cell-cell adhesion and permits escape from cell-cell contact-involved inhibition of cell growth. ..
  7. Davis J, Huang C, Zanet J, Harrison S, Rosten E, Cox S, et al. Emergence of embryonic pattern through contact inhibition of locomotion. Development. 2012;139:4555-60 pubmed publisher
    The pioneering cell biologist Michael Abercrombie first described the process of contact inhibition of locomotion more than 50 years ago when migrating fibroblasts were observed to rapidly change direction and migrate away upon collision...
  8. Anear E, Parish R. The effects of modifying RhoA and Rac1 activities on heterotypic contact inhibition of locomotion. FEBS Lett. 2012;586:1330-5 pubmed publisher
    b>Contact inhibition of locomotion (CIL) occurs when a cell ceases moving in the same direction following contact with another cell. Homotypic and heterotypic CIL occur between cells of the same and different types, respectively...
  9. Desai R, Gopal S, Chen S, Chen C. Contact inhibition of locomotion probabilities drive solitary versus collective cell migration. J R Soc Interface. 2013;10:20130717 pubmed publisher
    b>Contact inhibition of locomotion (CIL) is the process whereby cells collide, cease migrating in the direction of the collision, and repolarize their migration machinery away from the collision...
  10. Mancone C, Conti B, Amicone L, Bordoni V, Cicchini C, Calvo L, et al. Proteomic analysis reveals a major role for contact inhibition in the terminal differentiation of hepatocytes. J Hepatol. 2010;52:234-43 pubmed publisher
    ..Comparative proteomic analysis of proliferating versus quiescent hepatocytes validated the importance of contact inhibition, identifying 68 differently expressed gene products, representing 49 unique proteins...
  11. Schrader J, Deuster O, Rinn B, Schulz M, Kautz A, Dodel R, et al. Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown. BMC Cancer. 2009;9:464 pubmed publisher
    ..of proliferation under confluent and over-confluent conditions, implying a role of MIF in overcoming contact inhibition. Several proteins involved in contact inhibition including p27, p21, p53 and CEBPalpha are upregulated in ..
  12. Weiss C, Faust D, Schreck I, Ruff A, Farwerck T, Melenberg A, et al. TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A. Oncogene. 2008;27:2198-207 pubmed
    ..in transcriptional upregulation of the proto-oncogene cyclin A which finally triggers a release from contact inhibition. Ectopic expression of cyclin A in confluent cultures overcomes G(1) arrest, indicating that increased ..
  13. Hopfner R, Mousli M, Oudet P, Bronner C. Overexpression of ICBP90, a novel CCAAT-binding protein, overcomes cell contact inhibition by forcing topoisomerase II alpha expression. Anticancer Res. 2002;22:3165-70 pubmed
    ..Our results show that ICBP90 regulates topoisomerase II alpha expression and is able to overcome cell contact inhibition signaling, suggesting that increased ICBP90 expression may be involved in carcinogenesis.
  14. Machide M, Hashigasako A, Matsumoto K, Nakamura T. Contact inhibition of hepatocyte growth regulated by functional association of the c-Met/hepatocyte growth factor receptor and LAR protein-tyrosine phosphatase. J Biol Chem. 2006;281:8765-72 pubmed
    b>Contact inhibition, the inhibition of cell proliferation by tight cell-cell contact is a fundamental characteristic of normal cells...
  15. Uegaki K, Kanamori Y, Kigawa J, Kawaguchi W, Kaneko R, Naniwa J, et al. PTEN is involved in the signal transduction pathway of contact inhibition in endometrial cells. Cell Tissue Res. 2006;323:523-8 pubmed
    ..have shown that stable transfection of the PTEN gene into PTEN-mutated endometrial carcinoma cells leads to contact inhibition accompanied by a decreased level of phosphorylated-Akt (p-Akt) expression, an increase in p27(Kip1), and a ..
  16. Noseda M, Chang L, McLean G, Grim J, Clurman B, Smith L, et al. Notch activation induces endothelial cell cycle arrest and participates in contact inhibition: role of p21Cip1 repression. Mol Cell Biol. 2004;24:8813-22 pubmed
    ..We suggest that Notch activation contributes to contact inhibition of endothelial cells, in part through repression of p21Cip1 expression.
  17. Basan M, Idema T, Lenz M, Joanny J, Risler T. A reaction-diffusion model of the cadherin-catenin system: a possible mechanism for contact inhibition and implications for tumorigenesis. Biophys J. 2010;98:2770-9 pubmed publisher
    b>Contact inhibition is the process by which cells switch from a motile growing state to a passive and stabilized state upon touching their neighbors...
  18. Bosco E, Nakai Y, Hennigan R, Ratner N, Zheng Y. NF2-deficient cells depend on the Rac1-canonical Wnt signaling pathway to promote the loss of contact inhibition of proliferation. Oncogene. 2010;29:2540-9 pubmed publisher
    ..NF2) tumor suppressor gene encodes merlin, a membrane/cytoskeleton protein necessary for the maintenance of contact inhibition of growth in cells...
  19. Theveneau E, Marchant L, Kuriyama S, Gull M, Moepps B, Parsons M, et al. Collective chemotaxis requires contact-dependent cell polarity. Dev Cell. 2010;19:39-53 pubmed publisher
    ..These results show a role for N-cadherin during contact inhibition of locomotion, and they reveal a mechanism of chemoattraction likely to function during both embryogenesis ..
  20. Liu F, Jia L, Thompson Baine A, Puglise J, ter Beest M, Zegers M. Cadherins and Pak1 control contact inhibition of proliferation by Pak1-betaPIX-GIT complex-dependent regulation of cell-matrix signaling. Mol Cell Biol. 2010;30:1971-83 pubmed publisher
    ..of this complex from cell-matrix to cell-cell adhesion sites was required for the establishment of contact inhibition of proliferation. In this study, we provide evidence that this translocation depends on cadherin function...
  21. Aoki S, Diner E, de Roodenbeke C, Burgess B, Poole S, Braaten B, et al. A widespread family of polymorphic contact-dependent toxin delivery systems in bacteria. Nature. 2010;468:439-42 pubmed publisher
    ..Taken together, these results suggest that CDI systems constitute an intricate immunity network with an important function in bacterial competition. ..
  22. Kim N, Koh E, Chen X, Gumbiner B. E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components. Proc Natl Acad Sci U S A. 2011;108:11930-5 pubmed publisher
    b>Contact inhibition of cell growth is essential for embryonic development and maintenance of tissue architecture in adult organisms, and the growth of tumors is characterized by a loss of contact inhibition of proliferation...
  23. Chen H, Zhu Y, Chen S, Tseng S. Wnt signaling induces epithelial-mesenchymal transition with proliferation in ARPE-19 cells upon loss of contact inhibition. Lab Invest. 2012;92:676-87 pubmed publisher
    ..When contact inhibition of post-confluent ARPE-19 cells was disrupted by EGTA, an increase of BrdU labeling was noted only in the ..
  24. Chen H, Zhu Y, Chen S, Tseng S. Selective activation of p120ctn-Kaiso signaling to unlock contact inhibition of ARPE-19 cells without epithelial-mesenchymal transition. PLoS ONE. 2012;7:e36864 pubmed publisher
    ..RPE injury or degeneration may unlock mitotic block mediated by contact inhibition but may also promote epithelial-mesenchymal transition (EMT) contributing to retinal blindness...
  25. Zegers M, Forget M, Chernoff J, Mostov K, ter Beest M, Hansen S. Pak1 and PIX regulate contact inhibition during epithelial wound healing. EMBO J. 2003;22:4155-65 pubmed
    ..e. one that is not engaged in contact with neighboring cells. The Pak1 kinase mutants perturb contact inhibition by a mechanism that depends on the Pak-interacting Rac-GEF PIX...
  26. Grazia Lampugnani M, Zanetti A, Corada M, Takahashi T, Balconi G, Breviario F, et al. Contact inhibition of VEGF-induced proliferation requires vascular endothelial cadherin, beta-catenin, and the phosphatase DEP-1/CD148. J Cell Biol. 2003;161:793-804 pubmed
    ..Overall the data indicate that VE-cadherin-beta-catenin complex participates in contact inhibition of VEGF signaling...
  27. Zhao B, Wei X, Li W, Udan R, Yang Q, Kim J, et al. Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control. Genes Dev. 2007;21:2747-61 pubmed
    ..overexpression regulates gene expression in a manner opposite to cell density, and is able to overcome cell contact inhibition. Inhibition of YAP function restores contact inhibition in a human cancer cell line bearing deletion of ..
  28. Ota M, Sasaki H. Mammalian Tead proteins regulate cell proliferation and contact inhibition as transcriptional mediators of Hippo signaling. Development. 2008;135:4059-69 pubmed publisher
    ..overexpression, including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell contact inhibition and promotion of tumor formation...
  29. Nishi O, Yamamoto N, Nishi K, Nishi Y. Contact inhibition of migrating lens epithelial cells at the capsular bend created by a sharp-edged intraocular lens after cataract surgery. J Cataract Refract Surg. 2007;33:1065-70 pubmed
    ..To investigate whether the lens epithelial cells (LECs) at the capsular bend created by a sharp-edged intraocular lens (IOL) are in the G(0) phase of the cell cycle...
  30. McClatchey A, Yap A. Contact inhibition (of proliferation) redux. Curr Opin Cell Biol. 2012;24:685-94 pubmed publisher
    ..The mechanistic basis of contact inhibition of proliferation (CIP) has been slower to reveal itself...
  31. Gos M, Miloszewska J, Swoboda P, Trembacz H, Skierski J, Janik P. Cellular quiescence induced by contact inhibition or serum withdrawal in C3H10T1/2 cells. Cell Prolif. 2005;38:107-16 pubmed
    ..These results indicate that contact inhibition and serum withdrawal lead to cellular quiescence through distinct genetic and molecular mechanisms.
  32. Isaacson Wechsler E, Wang Q, Roberts I, Pagliarulo E, Jackson D, Untersperger C, et al. Reconstruction of human papillomavirus type 16-mediated early-stage neoplasia implicates E6/E7 deregulation and the loss of contact inhibition in neoplastic progression. J Virol. 2012;86:6358-64 pubmed publisher
    ..A reduced responsiveness to cell-cell contact inhibition and an increase in E6/E7 activity correlated closely with phenotype...
  33. Mayor R, Carmona Fontaine C. Keeping in touch with contact inhibition of locomotion. Trends Cell Biol. 2010;20:319-28 pubmed publisher
    b>Contact inhibition of locomotion (CIL) is the process by which cells in vitro change their direction of migration upon contact with another cell...
  34. Lee S, Lee S, Cho I, Oh M, Kang E, Kim Y, et al. Tetraspanin TM4SF5 mediates loss of contact inhibition through epithelial-mesenchymal transition in human hepatocarcinoma. J Clin Invest. 2008;118:1354-66 pubmed publisher
    The growth of normal cells is arrested when they come in contact with each other, a process known as contact inhibition. Contact inhibition is lost during tumorigenesis, resulting in uncontrolled cell growth...
  35. Sun X, Wang S, Zhang Y, Wang H, Wang L, Ying L, et al. Cell-cycle synchronization of fibroblasts derived from transgenic cloned cattle ear skin: effects of serum starvation, roscovitine and contact inhibition. Zygote. 2008;16:111-6 pubmed publisher
  36. Hneino M, Bouazza L, Bricca G, Li J, Langlois D. Density-dependent shift of transforming growth factor-beta-1 from inhibition to stimulation of vascular smooth muscle cell growth is based on unconventional regulation of proliferation, apoptosis and contact inhibition. J Vasc Res. 2009;46:85-97 pubmed publisher
    ..TGF-beta(1)-treated confluent vSMCs escaped contact inhibition and kept growing through unconventional regulation of p27(Kip1), cyclin E and suppression of apoptosis.
  37. Heckman C. Contact inhibition revisited. J Cell Physiol. 2009;220:574-5 pubmed publisher
    b>Contact inhibition of cell movement was originally defined in the 1950s as a way of interpreting studies that were ethological and statistical in nature...
  38. Davis P, Ho A, Dowdy S. Biological methods for cell-cycle synchronization of mammalian cells. Biotechniques. 2001;30:1322-6, 1328, 1330-1 pubmed
    ..other synchrony methods that involve less perturbation of biological systems, such as serum deprivation, contact inhibition, and centrifugal elutriation have a significant advantage...
  39. Aoki S, Webb J, Braaten B, Low D. Contact-dependent growth inhibition causes reversible metabolic downregulation in Escherichia coli. J Bacteriol. 2009;191:1777-86 pubmed publisher
    ..Consistent with the observed decrease in Deltap, the phage shock response was induced in cells undergoing CDI but not in recovering cells, based on analysis of levels of pspA mRNA. ..
  40. Gustincich S, Schneider C. Serum deprivation response gene is induced by serum starvation but not by contact inhibition. Cell Growth Differ. 1993;4:753-60 pubmed
    The relationship between quiescence induced by serum deprivation and that induced by high cell density (contact inhibition) is still unclear...
  41. Moore R, Theveneau E, Pozzi S, Alexandre P, Richardson J, Merks A, et al. Par3 controls neural crest migration by promoting microtubule catastrophe during contact inhibition of locomotion. Development. 2013;140:4763-75 pubmed publisher
    There is growing evidence that contact inhibition of locomotion (CIL) is essential for morphogenesis and its failure is thought to be responsible for cancer invasion; however, the molecular bases of this phenomenon are poorly understood...
  42. Theveneau E, Mayor R. Neural crest migration: interplay between chemorepellents, chemoattractants, contact inhibition, epithelial-mesenchymal transition, and collective cell migration. Wiley Interdiscip Rev Dev Biol. 2012;1:435-45 pubmed publisher
    ..recently identified, there is evidence that repulsive interactions between the cells, in a process called contact inhibition of locomotion, is one of the major driving forces behind directional migration...
  43. Nogueira V, Sundararajan D, Kwan J, Peng X, Sarvepalli N, Sonenberg N, et al. Akt-dependent Skp2 mRNA translation is required for exiting contact inhibition, oncogenesis, and adipogenesis. EMBO J. 2012;31:1134-46 pubmed publisher
    ..large T expression in Akt-deficient cells restores cell proliferation rate, but is insufficient for exiting contact inhibition and oncogene-induced anchorage-independent growth, because of a failure to promote Skp2 mRNA translation...
  44. Takai Y, Miyoshi J, Ikeda W, Ogita H. Nectins and nectin-like molecules: roles in contact inhibition of cell movement and proliferation. Nat Rev Mol Cell Biol. 2008;9:603-15 pubmed publisher
    ..alphavbeta3 and platelet-derived growth factor receptor, are crucial for the mechanisms that underlie contact inhibition of cell movement and proliferation; this has important implications for the development and tissue ..
  45. Aoki S, Pamma R, Hernday A, Bickham J, Braaten B, Low D. Contact-dependent inhibition of growth in Escherichia coli. Science. 2005;309:1245-8 pubmed
    ..The CdiAB system may function to regulate the growth of specific cells within a differentiated bacterial population. ..
  46. Faust D, Dolado I, Cuadrado A, Oesch F, Weiss C, Nebreda A, et al. p38alpha MAPK is required for contact inhibition. Oncogene. 2005;24:7941-5 pubmed
    ..importance for cell cycle control, knowledge about the intracellular signalling pathways involved in contact inhibition is scarce...
  47. Motti M, Califano D, Baldassarre G, Celetti A, Merolla F, Forzati F, et al. Reduced E-cadherin expression contributes to the loss of p27kip1-mediated mechanism of contact inhibition in thyroid anaplastic carcinomas. Carcinogenesis. 2005;26:1021-34 pubmed
    ..characterized several human thyroid cancer cell lines of different histotypes for their responsiveness to contact inhibition. We found that cells derived from differentiated carcinoma (TPC-1, WRO) arrest in G(1) phase at confluence, ..
  48. Anastasiadis P, Reynolds A. Regulation of Rho GTPases by p120-catenin. Curr Opin Cell Biol. 2001;13:604-10 pubmed
    ..The observations in these reports provide important new clues toward p120's mechanism of action and provide a potential explanation for the metastatic phenotype exhibited in carcinoma cells that have lost E cadherin expression. ..
  49. Ritt M, Mayor J, Wojcieszyn J, Smith R, Barton C, Modiano J. Sustained nuclear localization of p21/WAF-1 upon growth arrest induced by contact inhibition. Cancer Lett. 2000;158:73-84 pubmed
    We assessed the expression and distribution of p21/Waf-1 in TLM1 melanoma cells that exhibit contact inhibition and require serum for growth...
  50. Donaldson E, McKenna D, McMullen C, Scott W, Stitt A, Nelson J. The expression of membrane-associated 67-kDa laminin receptor (67LR) is modulated in vitro by cell-contact inhibition. Mol Cell Biol Res Commun. 2000;3:53-9 pubmed
    ..of retinal microvascular endothelial cells (RMEC) and in the breast cancer cell-line T47D during stages of contact inhibition. In both cell types, the expression levels of 67LR mRNA and membrane-associated 67LR protein were ..
  51. Astin J, Batson J, Kadir S, Charlet J, Persad R, Gillatt D, et al. Competition amongst Eph receptors regulates contact inhibition of locomotion and invasiveness in prostate cancer cells. Nat Cell Biol. 2010;12:1194-204 pubmed publisher
    ..Why cancer cells are defective in contact inhibition of locomotion is not understood...
  52. Kim S, Chin K, Gray J, Bishop J. A screen for genes that suppress loss of contact inhibition: identification of ING4 as a candidate tumor suppressor gene in human cancer. Proc Natl Acad Sci U S A. 2004;101:16251-6 pubmed
    We have devised a screen for genes that suppress the loss of contact inhibition elicited by overexpression of the protooncogene MYCN...
  53. Itano N, Atsumi F, Sawai T, Yamada Y, Miyaishi O, Senga T, et al. Abnormal accumulation of hyaluronan matrix diminishes contact inhibition of cell growth and promotes cell migration. Proc Natl Acad Sci U S A. 2002;99:3609-14 pubmed
    ..of HAS2 transfectants, suggesting that the intracellular PI3-kinase signaling regulates diminution of contact inhibition induced by formation of the massive hyaluronan matrix...