安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
10期
1400-1403,1404
,共5页
贾振亚%曹静%范文洁%徐玥%范璐璐%孙国平
賈振亞%曹靜%範文潔%徐玥%範璐璐%孫國平
가진아%조정%범문길%서모%범로로%손국평
肝癌%miR-107%增殖%细胞周期%CDK6
肝癌%miR-107%增殖%細胞週期%CDK6
간암%miR-107%증식%세포주기%CDK6
hepatocellular carcinoma%miR-107%proliferation%cell cycle%CDK6
目的探讨miR-107对HepG2细胞增殖和细胞周期的影响,以及对CDK6蛋白表达的调控。方法将50 nmol/L的miR-107 mimics 或阴性对照序列由 Lipofectamine 2000转染入人肝癌细胞株 HepG2中;qRT-PCR 法检测转染后HepG2细胞内miR-107表达水平;四甲基偶氮唑蓝( MTT)法检测细胞增殖能力;流式细胞术分析转染后细胞周期的变化;Western blot法检测CDK6蛋白表达水平。结果转染后24 h,miR-107 mimics转染组细胞内miR-107表达水平较空白对照组明显升高(P<0.05);与空白对照组相比,miR-107 mimics转染组HepG2细胞增殖受抑制( P<0.05),处于G0/G1期的细胞增多( P <0.05), CDK6蛋白表达下调( P <0.05)。结论 miR-107能够抑制 HepG2细胞增殖并诱导HepG2细胞G0/G1期阻滞,这可能与其抑制 CDK6蛋白的表达有关。
目的探討miR-107對HepG2細胞增殖和細胞週期的影響,以及對CDK6蛋白錶達的調控。方法將50 nmol/L的miR-107 mimics 或陰性對照序列由 Lipofectamine 2000轉染入人肝癌細胞株 HepG2中;qRT-PCR 法檢測轉染後HepG2細胞內miR-107錶達水平;四甲基偶氮唑藍( MTT)法檢測細胞增殖能力;流式細胞術分析轉染後細胞週期的變化;Western blot法檢測CDK6蛋白錶達水平。結果轉染後24 h,miR-107 mimics轉染組細胞內miR-107錶達水平較空白對照組明顯升高(P<0.05);與空白對照組相比,miR-107 mimics轉染組HepG2細胞增殖受抑製( P<0.05),處于G0/G1期的細胞增多( P <0.05), CDK6蛋白錶達下調( P <0.05)。結論 miR-107能夠抑製 HepG2細胞增殖併誘導HepG2細胞G0/G1期阻滯,這可能與其抑製 CDK6蛋白的錶達有關。
목적탐토miR-107대HepG2세포증식화세포주기적영향,이급대CDK6단백표체적조공。방법장50 nmol/L적miR-107 mimics 혹음성대조서렬유 Lipofectamine 2000전염입인간암세포주 HepG2중;qRT-PCR 법검측전염후HepG2세포내miR-107표체수평;사갑기우담서람( MTT)법검측세포증식능력;류식세포술분석전염후세포주기적변화;Western blot법검측CDK6단백표체수평。결과전염후24 h,miR-107 mimics전염조세포내miR-107표체수평교공백대조조명현승고(P<0.05);여공백대조조상비,miR-107 mimics전염조HepG2세포증식수억제( P<0.05),처우G0/G1기적세포증다( P <0.05), CDK6단백표체하조( P <0.05)。결론 miR-107능구억제 HepG2세포증식병유도HepG2세포G0/G1기조체,저가능여기억제 CDK6단백적표체유관。
Objective To investigate the effects of miR-107 on cell proliferation and cell cycle of HepG2 cells, as well as the expression of CDK 6 protein . Methods Human hepatoma HepG 2 cells were transfected with 50 nmol/L miR-107 mimics or negative control using Lipofectamine 2000. After transfection, the expression level of miR-107 was tested by qRT-PCR. Cell proliferation was tested by methylthiazol tetrazolium ( MTT) assay. Cell cycle was de-tected by flow cytometry. The expression level of CDK6 protein was measured by Western blot. Results Compared with the blank control group, the expression level of miR-107 in miR-107 mimics group was significantly increased (P<0.05). In addition, the proliferation of HepG2 cells was inhibited(P<0.05), G0/G1 phase cells were in-creased ( P<0.05 ) , and the expression level of CDK6 protein was decreased ( P <0.05 ) in miR-107 mimics group. Conclusion These results demonstrate that miR-107 inhibits the proliferation and induces G0/G1 phase ar-rest in HepG2 cells, which may be related to the inhibition of CDK6 expression.