中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
12期
2364-2366
,共3页
钟明珠%尧凯%董培%郭胜杰%周芳坚%韩辉
鐘明珠%堯凱%董培%郭勝傑%週芳堅%韓輝
종명주%요개%동배%곽성걸%주방견%한휘
前列腺癌%硒%缝隙连接蛋白
前列腺癌%硒%縫隙連接蛋白
전렬선암%서%봉극련접단백
Prostate cancer%Selenium%Connexin
目的 观察硒-甲基硒代半胱氨(MSC)对前列腺癌DU145细胞的缝隙连接蛋白43(Cx43)和细胞间隙连接通讯(GJIC)的影响及其作用.方法 0、5、10、25μmol/L MSC或转染CX43质粒处理前列腺癌DU145细胞,应用逆转录-聚合酶链反应(RT-PCR)和Western blot检测CX43mRNA和蛋白,划痕标记/染料示踪技术(SL/DT)检测GJIC功能,噻唑蓝(MTT)和克隆形成实验检测细胞生长和增殖能力,最后应用Western blot检测B淋巴细胞/白血病-2(bcl-2)蛋白水平.结果 5、10、25 μmol/L MSC均能上调DU145细胞CX43 mRNA和蛋白表达,且不增加GJIC功能,同时10、25 μmol/L MSC可以抑制DU145细胞生长和增殖(P<0.05);进一步在DU145细胞中过表达CX43,同样不增加GJIC功能,但可抑制DU145细胞生长和增殖(P<0.05).结论 MSC可诱导DU145细胞表达Cx43,且不增加GJIC功能,但能通过下调bcl-2抑制前列腺癌DU145细胞生长和增殖.
目的 觀察硒-甲基硒代半胱氨(MSC)對前列腺癌DU145細胞的縫隙連接蛋白43(Cx43)和細胞間隙連接通訊(GJIC)的影響及其作用.方法 0、5、10、25μmol/L MSC或轉染CX43質粒處理前列腺癌DU145細胞,應用逆轉錄-聚閤酶鏈反應(RT-PCR)和Western blot檢測CX43mRNA和蛋白,劃痕標記/染料示蹤技術(SL/DT)檢測GJIC功能,噻唑藍(MTT)和剋隆形成實驗檢測細胞生長和增殖能力,最後應用Western blot檢測B淋巴細胞/白血病-2(bcl-2)蛋白水平.結果 5、10、25 μmol/L MSC均能上調DU145細胞CX43 mRNA和蛋白錶達,且不增加GJIC功能,同時10、25 μmol/L MSC可以抑製DU145細胞生長和增殖(P<0.05);進一步在DU145細胞中過錶達CX43,同樣不增加GJIC功能,但可抑製DU145細胞生長和增殖(P<0.05).結論 MSC可誘導DU145細胞錶達Cx43,且不增加GJIC功能,但能通過下調bcl-2抑製前列腺癌DU145細胞生長和增殖.
목적 관찰서-갑기서대반광안(MSC)대전렬선암DU145세포적봉극련접단백43(Cx43)화세포간극련접통신(GJIC)적영향급기작용.방법 0、5、10、25μmol/L MSC혹전염CX43질립처리전렬선암DU145세포,응용역전록-취합매련반응(RT-PCR)화Western blot검측CX43mRNA화단백,화흔표기/염료시종기술(SL/DT)검측GJIC공능,새서람(MTT)화극륭형성실험검측세포생장화증식능력,최후응용Western blot검측B림파세포/백혈병-2(bcl-2)단백수평.결과 5、10、25 μmol/L MSC균능상조DU145세포CX43 mRNA화단백표체,차불증가GJIC공능,동시10、25 μmol/L MSC가이억제DU145세포생장화증식(P<0.05);진일보재DU145세포중과표체CX43,동양불증가GJIC공능,단가억제DU145세포생장화증식(P<0.05).결론 MSC가유도DU145세포표체Cx43,차불증가GJIC공능,단능통과하조bcl-2억제전렬선암DU145세포생장화증식.
Objective To study the effect of the Se-methylselenocysteine (MSC) treatment on Connexin 43 (Cx43) and gap junctional intercellular communication (GJIC) in the prostate cancer DU145 cells.Methods Cx43 mRNA and protein expression levels were examined by using reverse transcriptionpolymerase chain reaction (RT-PCR) and Western blotting,and GJIC function by the scrape-loading/dye transfer (SL/DT) after 0,5,10,25 μmol/L MSC treatment,respectively.The growth of prostate cancer DU145 cells was tested by using methyl thiazol tetrazolium (MTT) and clone formation assay,and the B lymphocytes/leukemia-2 (bcl-2) protein level by Western blotting after MSC treatment and Cx43 transfection.Results 5,10,and 25 μmol/L MSC or exogenous transfection of Cx43 in DU145 cells could induce the Cx43 mRNA and protein expression,but not the GJIC function.MSC treatment and up-regulation of Cx43 could reduce the bcl-2 level and inhibit the DU145 cell growth and proliferation (P < 0.05).Conclusion MSC can inhibit the DU145 cell growth and reduce the BCL-2 by up-regulating of Cx 43,which shows a new pathway of MSC in the anti-cancer effect.