中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
23期
4230-4233
,共4页
王劭晟%凌晓辉%吴永定%陈果%何绮微%江福能
王劭晟%凌曉輝%吳永定%陳果%何綺微%江福能
왕소성%릉효휘%오영정%진과%하기미%강복능
前列腺肿瘤%肿瘤侵润%细胞运动%miR-30c
前列腺腫瘤%腫瘤侵潤%細胞運動%miR-30c
전렬선종류%종류침윤%세포운동%miR-30c
Prostatic neoplasms%Neoplasm invasiveness%Cell movement%microRNA-30c
目的:研究miR-30c在前列腺癌中的功能调控作用,获得其调控前列腺癌侵袭及转移的可靠证据,进而揭示其在前列腺癌中可能的调控机制。方法从 miRNA 芯片检测结果中获得前列腺癌相关的差异表达的miR-30c分子,进一步通过miR-30c过表达质粒转染前列腺癌细胞,运用Transwell检测细胞侵袭变化,划痕实验检测细胞转移变化。结果 LNCaP/DU145转染质粒后, miR-30c的表达水平显著高于阴性对照组(LNCaP:倍数=3.87,P<0.001;Du145:倍数=4.32, P<0.001)。Transwell侵袭实验表明,miR-30c转染组的LNCaP/DU145细胞侵袭的数量显著低于对照组(LNCaP:67vs.120个/视野,P<0.001;DU145:130vs.220个/视野,P<0.001)。划痕实验结果发现miR-30c转染后,LNCaP/DU145细胞实验组转移的数量显著低于对照组(LNCaP:241 vs.520个/视野,P<0.001;DU145:490vs.660个/视野,P<0.001)。结论miR-30c可抑制前列腺癌细胞的侵袭及转移,这说明miR-30c在前列腺中确实起着抑癌的作用,其可能通过KRAS-MAPK信号通路抑制前列腺癌的侵袭及转移。
目的:研究miR-30c在前列腺癌中的功能調控作用,穫得其調控前列腺癌侵襲及轉移的可靠證據,進而揭示其在前列腺癌中可能的調控機製。方法從 miRNA 芯片檢測結果中穫得前列腺癌相關的差異錶達的miR-30c分子,進一步通過miR-30c過錶達質粒轉染前列腺癌細胞,運用Transwell檢測細胞侵襲變化,劃痕實驗檢測細胞轉移變化。結果 LNCaP/DU145轉染質粒後, miR-30c的錶達水平顯著高于陰性對照組(LNCaP:倍數=3.87,P<0.001;Du145:倍數=4.32, P<0.001)。Transwell侵襲實驗錶明,miR-30c轉染組的LNCaP/DU145細胞侵襲的數量顯著低于對照組(LNCaP:67vs.120箇/視野,P<0.001;DU145:130vs.220箇/視野,P<0.001)。劃痕實驗結果髮現miR-30c轉染後,LNCaP/DU145細胞實驗組轉移的數量顯著低于對照組(LNCaP:241 vs.520箇/視野,P<0.001;DU145:490vs.660箇/視野,P<0.001)。結論miR-30c可抑製前列腺癌細胞的侵襲及轉移,這說明miR-30c在前列腺中確實起著抑癌的作用,其可能通過KRAS-MAPK信號通路抑製前列腺癌的侵襲及轉移。
목적:연구miR-30c재전렬선암중적공능조공작용,획득기조공전렬선암침습급전이적가고증거,진이게시기재전렬선암중가능적조공궤제。방법종 miRNA 심편검측결과중획득전렬선암상관적차이표체적miR-30c분자,진일보통과miR-30c과표체질립전염전렬선암세포,운용Transwell검측세포침습변화,화흔실험검측세포전이변화。결과 LNCaP/DU145전염질립후, miR-30c적표체수평현저고우음성대조조(LNCaP:배수=3.87,P<0.001;Du145:배수=4.32, P<0.001)。Transwell침습실험표명,miR-30c전염조적LNCaP/DU145세포침습적수량현저저우대조조(LNCaP:67vs.120개/시야,P<0.001;DU145:130vs.220개/시야,P<0.001)。화흔실험결과발현miR-30c전염후,LNCaP/DU145세포실험조전이적수량현저저우대조조(LNCaP:241 vs.520개/시야,P<0.001;DU145:490vs.660개/시야,P<0.001)。결론miR-30c가억제전렬선암세포적침습급전이,저설명miR-30c재전렬선중학실기착억암적작용,기가능통과KRAS-MAPK신호통로억제전렬선암적침습급전이。
ObjectiveTo study the function of miR-30c which may regulate prostate cancer progression, and we get the reliable evidence that miR-30c regulates the invasion and metastasis of prostate cancer, reveals the possible regulatory mechanism in prostate cancer.MethodsWe chose miR-30c from the differentially expressed miRNAs through miRNA microarray on the human samples. Further by miR-30c overexpression plasmid transfecting prostate cancer cells, using Transwell test cell invasion changed, wound healing test cells shift change.ResultsThe miR-30c expression levels were measured at 48 hours after transfection by qRT-PCR. Data showed that miR-30c expression level in miR-30c-transfected cells was significantly increased compared that in control cells (LNCaP, fold=3.87, P<0.01; Du145, fold=4.32,P<0.01). The results of Transwell assay clearly revealed that overexpression of miR-30c significantly reduced the migrated miR-30c-transfected LNCaP and DU145 cells compared with control cells (LNCaP: 67vs. 120 cells/field,P<0.01; DU145: 130vs. 220 cells/field,P<0.01). The results of wound healing assay indicated that miR-30c markedly reduced the migration of LNCaP and DU145 cells (LNCaP: 241vs. 520 cells/field,P<0.01; DU145: 490vs. 660 cells/field,P<0.01).ConclusionmiR-30c can inhibit invasion and migration of prostate cancer cells, which proved miR-30c can serve as tumor suppressor, and KRAS-MAPK pathway may be involved.