中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
9期
2160-2162
,共3页
宋军%樊瑞智%徐溢新%宋虎%付海啸%白津%郑骏年%徐为
宋軍%樊瑞智%徐溢新%宋虎%付海嘯%白津%鄭駿年%徐為
송군%번서지%서일신%송호%부해소%백진%정준년%서위
胃癌%微小RNA-30a%增殖%迁移%侵袭
胃癌%微小RNA-30a%增殖%遷移%侵襲
위암%미소RNA-30a%증식%천이%침습
Gastric carcinoma%MicroRNA-30a%Proliferation%Migration%Invasion
目的 观察微小RNA-30a(miR-30a)对胃癌细胞生物学行为的影响.方法 将miR-30a模拟物及抑制物瞬时转染胃癌细胞株SGC7901,实验分未转染组、空白对照组、miR-30a模拟物转染组、miR-30a抑制物转染组4组,实时定量反转录聚合酶链反应(RT-qPCR)检测miR-30a的表达水平,细胞计数试剂盒(CCK-8)法检测细胞增殖能力,流式细胞术检测细胞凋亡及细胞周期,Transwell小室检测细胞体外侵袭迁移能力.结果 与两对照组比较,胃癌SGC7901细胞在转染模拟物后,miR-30a表达明显上调,而转染抑制物后miR-30a表达明显受抑,差异有统计学意义(P<0.叭).与对照组及抑制物转染组比较,miR-30a模拟物转染组细胞增殖活性、迁移和侵袭能力相对减弱(P<0.05),而细胞凋亡率[(32.1±2.1)%]较未转染组[(18.8±1.2)%]、空白对照组[(18.6±1.1)%]和抑制物转染组[(16.4±1.9)%]增加(P<0.05),细胞周期S期增多达(36.7±3.6)%,出现S期阻滞.结论 miR-30a可明显抑制胃癌细胞株SGC7901的增殖,促进其凋亡,抑制其迁移及侵袭能力.
目的 觀察微小RNA-30a(miR-30a)對胃癌細胞生物學行為的影響.方法 將miR-30a模擬物及抑製物瞬時轉染胃癌細胞株SGC7901,實驗分未轉染組、空白對照組、miR-30a模擬物轉染組、miR-30a抑製物轉染組4組,實時定量反轉錄聚閤酶鏈反應(RT-qPCR)檢測miR-30a的錶達水平,細胞計數試劑盒(CCK-8)法檢測細胞增殖能力,流式細胞術檢測細胞凋亡及細胞週期,Transwell小室檢測細胞體外侵襲遷移能力.結果 與兩對照組比較,胃癌SGC7901細胞在轉染模擬物後,miR-30a錶達明顯上調,而轉染抑製物後miR-30a錶達明顯受抑,差異有統計學意義(P<0.叭).與對照組及抑製物轉染組比較,miR-30a模擬物轉染組細胞增殖活性、遷移和侵襲能力相對減弱(P<0.05),而細胞凋亡率[(32.1±2.1)%]較未轉染組[(18.8±1.2)%]、空白對照組[(18.6±1.1)%]和抑製物轉染組[(16.4±1.9)%]增加(P<0.05),細胞週期S期增多達(36.7±3.6)%,齣現S期阻滯.結論 miR-30a可明顯抑製胃癌細胞株SGC7901的增殖,促進其凋亡,抑製其遷移及侵襲能力.
목적 관찰미소RNA-30a(miR-30a)대위암세포생물학행위적영향.방법 장miR-30a모의물급억제물순시전염위암세포주SGC7901,실험분미전염조、공백대조조、miR-30a모의물전염조、miR-30a억제물전염조4조,실시정량반전록취합매련반응(RT-qPCR)검측miR-30a적표체수평,세포계수시제합(CCK-8)법검측세포증식능력,류식세포술검측세포조망급세포주기,Transwell소실검측세포체외침습천이능력.결과 여량대조조비교,위암SGC7901세포재전염모의물후,miR-30a표체명현상조,이전염억제물후miR-30a표체명현수억,차이유통계학의의(P<0.팔).여대조조급억제물전염조비교,miR-30a모의물전염조세포증식활성、천이화침습능력상대감약(P<0.05),이세포조망솔[(32.1±2.1)%]교미전염조[(18.8±1.2)%]、공백대조조[(18.6±1.1)%]화억제물전염조[(16.4±1.9)%]증가(P<0.05),세포주기S기증다체(36.7±3.6)%,출현S기조체.결론 miR-30a가명현억제위암세포주SGC7901적증식,촉진기조망,억제기천이급침습능력.
Objective To explore the effect of microRNA-30a (miR-30a) on the biological behaviors of human gastric carcinoma cells.Methods Experiments were divided into four groups:negative control group and blank control group,miR-30a mimics group,miR-30a inhibitor group.miR-30a mimics group was transfected with miR-30a mimics to enhance the functions of miR-30a,and miR-30a inhibitor group was transfected with miR-30a inhibitor.miR-30a mRNA expression was detected by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR).Cell proliferation was evaluated using the cell counting kit-8 (CCK-8) assay and apoptosis was assessed by flow cytometry.Invasion and migration were measured by Transwell chamber assays.Results The SGC7901 cells transfected with miR-30a mimics showed significantly higher miR-30a mRNA expression than the non-transfected SGC7901 cells and the transfected control cells (P < 0.01).The miR-30a mRNA expression was significantly lower in the SGC7901 cells transfected with the miR-30a inhibitor than the non-transfected SGC7901 cells and the transfected control cells (P < 0.01).The overexpression of miR-30a inhibited the viability and invasion and migration abilities,as shown in the cells transfected with the miR-30a mimics (P < 0.05).There was no significant difference between control group and blank group,and the apoptosis rate in the experimental group [(32.1 ± 2.1) %] was significantly higher than that in the control group [(18.8 ± 1.2) %],blank group [(18.6 ± 1.1) %] and inhibitor group [(16.4 ± 1.9) %] (P < 0.05),and the cell cycle was significantly arrested in S phase and the number of S phase cells was increased larger than (36.7 ± 3.6) % by flow cytometry.Conclusion miR-30a had an inhibitory effect on cell proliferation,induced apoptosis,and markedly inhibited invasion and migration of SGC7901 cells.