You have accessJournal of UrologyProstate Cancer: Basic Research V1 Apr 2014MP52-16 EXPRESSION OF CYTEINE-RICH 61 IS INDUCED BY EXTRACELLULAR ACIDIFICATION WITH PI3K/AKT ACTIVATION AND CONTRIBUTES TO MALIGNANT PHENOTYPES OF PROSTATE CARCINOMA CELLS Changho Lee, Yoon-Jin Lee, Hee Jo Yang, Doo Sang Kim, Youn Soo Jeon, and Sang-Han Lee Changho LeeChangho Lee More articles by this author , Yoon-Jin LeeYoon-Jin Lee More articles by this author , Hee Jo YangHee Jo Yang More articles by this author , Doo Sang KimDoo Sang Kim More articles by this author , Youn Soo JeonYoun Soo Jeon More articles by this author , and Sang-Han LeeSang-Han Lee More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.1626AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail Introduction and Objectives High expression of cysteine-rich 61 (Cyr61) has been associated with a malignant cell phenotype and poor outcome in prostate cancer. The aim of this study is to elucidate the condition around Cyr61 expression and investigate the effect of inhibiting Cyr61 expression using small interfering RNA (siRNA) on the proliferation, migration and invasion. Methods RNA interference of Cyr61 was performed using a Cyr61-specific siRNA duplex. Cell proliferation was measured by XTT assay. Apoptosis assay, colony formation assay, wound healing assay and Matrigel invasion assay were examined. Results Extracellular acidification induced Cyr61 expression in androgen-independent PC-3 cells. Silencing of Cyr61 by siRNA inhibited cell proliferation with enhanced activity of caspase-3/7, upregulation of the proapoptotic Bok, BimL and BimS, cleavage of apoptosis hallmarkers such as Bax, PARP and caspase-3, and downregulation of antiapoptotic Bcl2, Bcl-xL and Mcl-1 proteins. siRNA-based silencing of Cyr61 resulted in the decrease of colony-formation capacity, migration and invasion. At the same time, Cyr61 silencing effectively reduced the levels of phosphorylated Akt and integrin-β3. Conclusions Our data indicate that PC-3 cells overproduce Cyr61 as a part of the survival mechanisms under the conditions causing extracellular acidity. Cyr61 modulates integrin-β3 level as well as PI3-kinase/Akt activity through which Cyr61 may mediate tumorigenesis and metastasis. It also suggest the potential importance of Cyr61 targeting on enhancing the therapeutic efficacy of prostate cancer. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e586 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Changho Lee More articles by this author Yoon-Jin Lee More articles by this author Hee Jo Yang More articles by this author Doo Sang Kim More articles by this author Youn Soo Jeon More articles by this author Sang-Han Lee More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...