Relationship Between Expression Of HSPC111 And Radiosensitivity In Prostate Cancer

ObjectiveTo investigate the expression of HSPC111 in prostate cancer.In vitro test we discuss the impact of HSPC111 on biological behiviors of prostate cancer PC3 cell.To explore HSPC111’s influence on the progression of prostate cancer.To investigate the relationship between HSPC111 and the sensitivity of radiotherapy in prostate cancer and its mechanisms.MethodsThe polymerase chain reaction and Western Blot were used to detect the expression of HSPC111 in the cell line of PC3 and RWPE-1in,PCa tissue and benign prostatic hyperplasia tissue.We transduced the HSPC111 shRNA Lentiviral Particles to transduced into PC3 cells.Select cell with stable low expression of HSPC111 by Puromycin selection and monocolon picking.The expression of HSPC111 in transduced PC3 cells were tested by the polymerase chain reaction and Western Blot.After transfection we use MTT assay method to test the proliferation of cells.We use Transwell assay to test invasion of PC3 cells.Apoptosis and Cell cycle distribution of PC3 cell were evaluated by flow cytometry.And then we give the radiation therapy on PC3 cell.The radiosensitivity of PC3 cells were detect by clone formation.The effect of HSPC111 on cell cycle and apoptosis distribution of PC3 cells with X-ray was detected by flow cytometry.The effect of HSPC111 on expression of protein related with apoptosis and DNA damage repair proteins in PC3 cells with X-ray was analyzed by Western blot.The expression of γ-H2 AX caused by radiation was tested by Western blot.The effect of HSPC111 on tumor-burdened nude mice tumor sensitivity to radiotherapy was detected in vivo test.ResultsThe expression of HSPC111 in prostate cancer tissues increased;In prostate cancer cells PC3 the expression of HSPC111 is higher than prostate cells RWPE-1.Use stable low expression of HSPC111 virus transfect PC3 cells can reduce the expression levels of HSPC111.In vitro cell biology behavior detection,cut HSPC111 expression level can decrease the cell proliferation of PC3 cells.Can make the PC3 prostate cancer cells invasion ability decreased obviously.Can increase ability of apoptosis inPC3 cells.Block the cell cycle in G0/G1,reduce the replication of DNA,wich affect cell proliferation.On cell clone formation experiment,the results show that after different doses of X-ray irradiation,the survival curve of HSPC111 lower expression of PC3 decreased significantly,its SF2 D0 and N also decreased significantly,general sensitization enhancing ratio were 2.22.Further study showed that radiation exposure can make cell crcle arrest in G2/M phase,increase cells apoptosis of PC3,increase the expression of apoptosis related proteins of Caspase-8 and decrease the expression of antiapoptotic protein Bcl-2,increase the expression of DNA damage markers γ-H2 AX and DNA damage repair protein Ku80.Cut HSPC111 expression can reduce radiation caused G2/M arrest;Promote the apoptosis caused by radiation;Promote the expression of Caspase-8 caused by radiation;Inhibite the expression of Bcl-2 caused by radiation;Inhibite the expression of ku80 caused by radiation and promote the expression of γ-H2 AX.In vivo tests,both tumor reduction experiment and tumor growth curve experiment showed that HSPC111 lower expression can increase the nude mice tumor radiotherapy sensitivity.ConclusionThe expression of HSPC111 in prostate cancer is high.Reduce the expression of HSPC111 can reduce PC3 cells proliferation,promote apoptosis,reduce its ability to attack.We believe that lower HSPC111 expression can restrain the progress of prostate cancer.Cut the expression of HSPC111 can increase the radiosensitivity of PC3 cells.Nude mice experiments further confirmed that cut expression of HSPC111 synergy radiation therapy can inhibit tumor growth.Its mechanism may be to regulation of cell cycle and apoptosis,regulating apoptosis related proteins and DNA damage repair protein expression,thus reducing the radiation induced G2 / M phase retardation,reduce DNA damage repair ability,increase cell apoptosis.