东南大学学报(医学版)
東南大學學報(醫學版)
동남대학학보(의학판)
JOURNAL OF SOUTHEAST UNIVERSITY(MEDICAL SCIENCE EDITION)
2015年
3期
337-341
,共5页
刘大闯%梁清%陶陶%黄烨清%许斌%陈恕求%张治国%董洋%韩从辉%陈明
劉大闖%樑清%陶陶%黃燁清%許斌%陳恕求%張治國%董洋%韓從輝%陳明
류대틈%량청%도도%황엽청%허빈%진서구%장치국%동양%한종휘%진명
前列腺癌%特殊蛋白1%细胞增殖%丙酮酸激酶同工酶M2型%有氧糖酵解
前列腺癌%特殊蛋白1%細胞增殖%丙酮痠激酶同工酶M2型%有氧糖酵解
전렬선암%특수단백1%세포증식%병동산격매동공매M2형%유양당효해
prostate cancer%specificity protein 1%cell proliferation%pyruvate kinase isoenzyme type M 2%aerobic glycolysis
目的:确定前列腺癌中Sp1通过PKM2途径对前列腺癌细胞的增殖和代谢的作用。方法:前列腺癌细胞株DU145与PC3体外转染Sp1 siRNA与阴性对照无意义核苷酸序列( NC组),采用葡萄糖检测试剂盒与乳酸检测试剂盒检测转染后有氧糖酵解变化;CCK-8实验检测转染后的细胞增殖;qRT-PCR检测转染后PKM2表达;Western Blotting检测转染后Sp1与PKM2表达。结果:DU145与PC3转染Sp1 siRNA后与NC组比较,剩余葡萄糖显著偏高,乳酸产生显著下降;CCK8实验表明抑制Sp1后能显著抑制前列腺癌细胞的增殖能力;qRT-PCR实验显示抑制Sp1后明显抑制PKM2的表达;Western Blotting 显示转染的Sp1 siRNA对Sp1具有较高的沉默效率,且PKM2的表达也降低。结论:Sp1在前列腺癌细胞株DU145与PC3中可通过直接作用于PKM2促进细胞代谢。
目的:確定前列腺癌中Sp1通過PKM2途徑對前列腺癌細胞的增殖和代謝的作用。方法:前列腺癌細胞株DU145與PC3體外轉染Sp1 siRNA與陰性對照無意義覈苷痠序列( NC組),採用葡萄糖檢測試劑盒與乳痠檢測試劑盒檢測轉染後有氧糖酵解變化;CCK-8實驗檢測轉染後的細胞增殖;qRT-PCR檢測轉染後PKM2錶達;Western Blotting檢測轉染後Sp1與PKM2錶達。結果:DU145與PC3轉染Sp1 siRNA後與NC組比較,剩餘葡萄糖顯著偏高,乳痠產生顯著下降;CCK8實驗錶明抑製Sp1後能顯著抑製前列腺癌細胞的增殖能力;qRT-PCR實驗顯示抑製Sp1後明顯抑製PKM2的錶達;Western Blotting 顯示轉染的Sp1 siRNA對Sp1具有較高的沉默效率,且PKM2的錶達也降低。結論:Sp1在前列腺癌細胞株DU145與PC3中可通過直接作用于PKM2促進細胞代謝。
목적:학정전렬선암중Sp1통과PKM2도경대전렬선암세포적증식화대사적작용。방법:전렬선암세포주DU145여PC3체외전염Sp1 siRNA여음성대조무의의핵감산서렬( NC조),채용포도당검측시제합여유산검측시제합검측전염후유양당효해변화;CCK-8실험검측전염후적세포증식;qRT-PCR검측전염후PKM2표체;Western Blotting검측전염후Sp1여PKM2표체。결과:DU145여PC3전염Sp1 siRNA후여NC조비교,잉여포도당현저편고,유산산생현저하강;CCK8실험표명억제Sp1후능현저억제전렬선암세포적증식능력;qRT-PCR실험현시억제Sp1후명현억제PKM2적표체;Western Blotting 현시전염적Sp1 siRNA대Sp1구유교고적침묵효솔,차PKM2적표체야강저。결론:Sp1재전렬선암세포주DU145여PC3중가통과직접작용우PKM2촉진세포대사。
Objective: To determine wether the Sp1 could accelerate the metabolism of prostate cancer cells through PKM2.Methods:DU145 and PC3 cell lines of prostate cancer were transfected with Sp 1 siRNA or NC. Aerobic glycolysis was detected by the glucose and lactic acid detection kit after transfection .Cell proliferation was detected by CCK-8 assay.PKM2 mRNA expression was detected by qRT-PCR.Sp1or PKM2 expression was tested by Western Blotting .Results:The remaining glucose level was higher in Sp 1 siRNA group than in NC group , the lactic acid level declined significantly after Sp1 siRNA transfection.CCK-8 assay revealed over-expression of Sp1 siRNA significantly inhibited proliferation .qRT-PCR showed that the inhibition of Sp 1 could significantly inhibit the expression of PKM2.Western Blotting showed that Sp 1 had high efficiency of silence , PKM2 expression reduced significantly after Sp 1 siRNA reansfection .Conclusion: Sp1 acts directly on PKM2 to promote cell metabolism in DU145 and PC3 cell lines of prostate cancer .