Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.biocel.2007.06.020
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dc.titleCyr61/CCN1 is a tumor suppressor in human hepatocellular carcinoma and involved in DNA damage response
dc.contributor.authorFeng, P.
dc.contributor.authorRen, E.C.
dc.contributor.authorWang, B.
dc.date.accessioned2011-07-26T06:54:12Z
dc.date.available2011-07-26T06:54:12Z
dc.date.issued2008
dc.identifier.citationFeng, P., Ren, E.C., Wang, B. (2008). Cyr61/CCN1 is a tumor suppressor in human hepatocellular carcinoma and involved in DNA damage response. International Journal of Biochemistry and Cell Biology 40 (1) : 98-109. ScholarBank@NUS Repository. https://doi.org/10.1016/j.biocel.2007.06.020
dc.identifier.issn13572725
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/24757
dc.description.abstractCyr61/CCN1 is a secreted extracellular matrix associated protein involved in diverse biological functions and plays multiple roles in tumorigenesis. Cyr61 was down-regulated in HCC tumor tissues as observed in our previous cDNA microarray study, but its potential role in hepatocarcinogenesis is still unclear. To explore the biological significance of Cyr61 in HCC development, over-expression of this gene was established in HCC cell lines and its effects on cell proliferation, adhesion, migration and invasion were analyzed in this study. Cyr61 expression was down-regulated in HCC tumors as measured by quantitative real-time PCR and its protein level was decreased in most HCC cell lines as detected by Western blot. Over-expression of Cyr61 in HCC cell lines suppressed cell proliferation in monolayer and anchorage-independent growth in soft agar, whereas down-regulation of Cyr61 by siRNA increased cell proliferation rate. Over-expression of Cyr61 also significantly enhanced adhesion activities of HepG2 cells to various ECM proteins. Moreover, stably transfected HepG2-Cyr61 cells showed inhibited cell mobility (40-45%) and reduced invasiveness (30-40%) compared to HepG2-Neo controls. Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53+/+ HepG2 and p53-/- Hep3B cells. However, only HepG2 cells showed increased G2/M phase arrest with concomitant up-regulation in p53 and p21 levels, suggesting that Cyr61 may play an active role in regulating HCC cell growth involving p53 as well as alternative pathways. In conclusion, we demonstrated that Cyr61 is a tumor suppressor in hepatocarcinogenesis and is involved in DNA damage response. © 2007 Elsevier Ltd. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.biocel.2007.06.020
dc.sourceScopus
dc.subjectCyr61
dc.subjectGenotoxic stress
dc.subjectHepatocellular carcinoma
dc.subjectp53
dc.subjectTumor suppressor
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1016/j.biocel.2007.06.020
dc.description.sourcetitleInternational Journal of Biochemistry and Cell Biology
dc.description.volume40
dc.description.issue1
dc.description.page98-109
dc.identifier.isiut000251461800010
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