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Low expression of microRNA-30c promotes prostate cancer cells invasion involved in downregulation of KRAS protein.

ABSTRACT: Aberrant microRNA expression is associated with tumor development. The present study aimed to elucidate the role of miR-30c in the development of prostate cancer. Quantitative polymerase chain reaction was performed to compare miR-30c expression in LNCaP, DU145, PC-3 and RWPE-1 cell lines. Lentivirus expressing miR-30c was used to create stable overexpression cell lines to investigate the effects of miR-30c overexpression on cell proliferation, migration and invasion, which were determined in the prostate cancer cell line PC-3 by MTT, colony formation, wound healing and Transwell assays. Effects of miR-30c on KRAS were examined by western blot analysis. miR-30c expression was significantly lower (P<0.05) in the PC-3 cell line compared with LNCaP, DU145 and RWPE-1 cell lines. miR-30c overexpression in PC-3 inhibited tumor cell proliferation, migration and invasion in vitro. Furthermore, KRAS protein expression was downregulated in miR-30c overexpression cell lines compared with the negative control (NC) group (P<0.05). The present results demonstrated that overexpression of miR-30c inhibits prostate cancer cell line proliferation, migration and invasion, which was possibly caused by downregulation of KRAS protein by miR-30c. The data implicate miR-30c in the prognosis and treatment of prostate cancer.

SUBMITTER: Zhang J

PROVIDER: S-EPMC5494817 | biostudies-other | 2017 Jul

REPOSITORIES: biostudies-other

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Project description:BackgroundProstate cancer is the most common form of cancer in males and accounts for high cancer related deaths. Therapeutic advancement in prostate cancer has not been able to reduce the mortality burden of prostate cancer, which warrants further research. FRG1 which affects angiogenesis and cell migration in Xenopus, can be a potential player in tumorigenesis. In this study, we investigated the role of FRG1 in prostate cancer progression.MethodsImmunohistochemistry was performed to determine FRG1 expression in patient samples. FRG1 expression perturbation was done to investigate the effect of FRG1 on cell proliferation, migration and invasion, in DU145, PC3 and LNCaP cells. To understand the mechanism, we checked expression of various cytokines and MMPs by q-RT PCR, signaling molecules by western blot, in FRG1 perturbation sets. Results were validated by use of pharmacological inhibitor and activator and, western blot.ResultsIn prostate cancer tissue, FRG1 levels were significantly reduced, compared to the uninvolved counterpart. FRG1 expression showed variable effect on PC3 and DU145 cell proliferation. FRG1 levels consistently affected cell migration and invasion, in both DU145 and PC3 cells. Ectopic expression of FRG1 led to significant reduction in cell migration and invasion in both DU145 and PC3 cells, reverse trends were observed with FRG1 knockdown. In androgen receptor positive cell line LNCaP, FRG1 doesn't affect any of the cell properties. FRG1 knockdown led to significantly enhanced expression of GM-CSF, MMP1, PDGFA and CXCL1, in PC3 cells and, in DU145, it led to higher expression of GM-CSF, MMP1 and PLGF. Interestingly, FRG1 knockdown in both the cell lines led to activation of p38 MAPK. Pharmacological activation of p38 MAPK led to increase in the expression of GM-CSF and PLGF in DU145 whereas in PC3 it led to enhanced expression of GM-CSF, MMP1 and CXCL1. On the other hand, inhibition of p38 MAPK led to reduction in the expression of above mentioned cytokines.ConclusionFRG1 expression is reduced in prostate adenocarcinoma tissue. FRG1 expression affects migration and invasion in AR negative prostate cancer cells through known MMPs and cytokines, which may be mediated primarily via p38 MAPK activation.

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Low expression of microRNA-30c promotes prostate cancer cells invasion involved in downregulation of KRAS protein.

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