温州医科大学学报
溫州醫科大學學報
온주의과대학학보
Journal of Wenzhou Medical University
2015年
4期
235-239
,共5页
诸梦露%刘婷婷%彭晓丹%林绍强
諸夢露%劉婷婷%彭曉丹%林紹彊
제몽로%류정정%팽효단%림소강
唾液酸转移酶%胃肿瘤%唾液酸化%增殖%迁移
唾液痠轉移酶%胃腫瘤%唾液痠化%增殖%遷移
타액산전이매%위종류%타액산화%증식%천이
ST6Gal I%stomach neoplasms%sialylation%proliferation%migration
目的:探讨唾液酸转移酶(ST6Gal I)对人胃癌细胞(SGC7901)增殖和迁移能力的影响。方法:采用脂质体2000(Lipofectamine 2000),构建ST6Gal I高表达和ST6Gal I低表达细胞株,以空载体(Vector)作为对照组。采用实时荧光定量PCR(real-time PCR,RT-PCR)检测转染后SGC7901细胞中ST6Gal I的mRNA水平;用细胞CCK-8试剂盒及Transwell小室实验检测转染前后细胞的增殖、迁移情况。结果:成功构建稳定转染单克隆细胞株分别为Vector、X61-4和PS7;与Vector组相比,PS7组的mRNA表达水平显著增加(P<0.05),X61-4组则显著降低(P<0.05);X61-4的细胞增殖明显高于PS7细胞(P<0.05);胃癌细胞ST6Gal I的表达水平与细胞迁移能力成正相关,PS7组的迁移率显著高于X61-4组(P<0.01)和Vector组(P<0.01), X61-4组的迁移率低于Vector组(P<0.05)。结论:细胞实验表明,降低ST6Gal I的表达可以有效促进胃癌SGC7901细胞的增殖能力,而上调ST6Gal I可以增强胃癌细胞的迁移能力。因此,ST6Gal I是与肿瘤增殖和转移相关的基因,是潜在的肿瘤分子治疗靶点。
目的:探討唾液痠轉移酶(ST6Gal I)對人胃癌細胞(SGC7901)增殖和遷移能力的影響。方法:採用脂質體2000(Lipofectamine 2000),構建ST6Gal I高錶達和ST6Gal I低錶達細胞株,以空載體(Vector)作為對照組。採用實時熒光定量PCR(real-time PCR,RT-PCR)檢測轉染後SGC7901細胞中ST6Gal I的mRNA水平;用細胞CCK-8試劑盒及Transwell小室實驗檢測轉染前後細胞的增殖、遷移情況。結果:成功構建穩定轉染單剋隆細胞株分彆為Vector、X61-4和PS7;與Vector組相比,PS7組的mRNA錶達水平顯著增加(P<0.05),X61-4組則顯著降低(P<0.05);X61-4的細胞增殖明顯高于PS7細胞(P<0.05);胃癌細胞ST6Gal I的錶達水平與細胞遷移能力成正相關,PS7組的遷移率顯著高于X61-4組(P<0.01)和Vector組(P<0.01), X61-4組的遷移率低于Vector組(P<0.05)。結論:細胞實驗錶明,降低ST6Gal I的錶達可以有效促進胃癌SGC7901細胞的增殖能力,而上調ST6Gal I可以增彊胃癌細胞的遷移能力。因此,ST6Gal I是與腫瘤增殖和轉移相關的基因,是潛在的腫瘤分子治療靶點。
목적:탐토타액산전이매(ST6Gal I)대인위암세포(SGC7901)증식화천이능력적영향。방법:채용지질체2000(Lipofectamine 2000),구건ST6Gal I고표체화ST6Gal I저표체세포주,이공재체(Vector)작위대조조。채용실시형광정량PCR(real-time PCR,RT-PCR)검측전염후SGC7901세포중ST6Gal I적mRNA수평;용세포CCK-8시제합급Transwell소실실험검측전염전후세포적증식、천이정황。결과:성공구건은정전염단극륭세포주분별위Vector、X61-4화PS7;여Vector조상비,PS7조적mRNA표체수평현저증가(P<0.05),X61-4조칙현저강저(P<0.05);X61-4적세포증식명현고우PS7세포(P<0.05);위암세포ST6Gal I적표체수평여세포천이능력성정상관,PS7조적천이솔현저고우X61-4조(P<0.01)화Vector조(P<0.01), X61-4조적천이솔저우Vector조(P<0.05)。결론:세포실험표명,강저ST6Gal I적표체가이유효촉진위암SGC7901세포적증식능력,이상조ST6Gal I가이증강위암세포적천이능력。인차,ST6Gal I시여종류증식화전이상관적기인,시잠재적종류분자치료파점。
Objective: To explore the effect of α2, 6 sialytransferase (ST6Gal I) on the abilities of proliferation and migration in SGC7901 cells. Methods: Gastric cancer cell lines SGC7901 were con-structed to ST6Gal I high expression (PS7) and ST6Gal I lower expression (X61) with lipofectamine 2000 and empty vector (Vector) was used as a control group. The expression of ST6Gal I was examined with RT-PCR. Cell proliferation was evaluated with the CCK-8 kit, and migration was evaluated with Transwell chamber assay. Results: The 3 stable transfected cell lines were constructed successfully. The most effec-tive clone cells were chosed as our experimental cells, and named as Vector, X61-4 and PS7. In contrasted with Vector, the expression of ST6GAL I in X61-4 was statistically significant lower (P<0.05), and PS7 was statistically significant higher (P<0.05). Cell growth curve showed that cell proliferation of X61-4 was obviously higher than that of PS7 cells (P<0.05). The transwell chamber assay results showed that the migra-tion of PS7 was signiifcantly higher than that of the X61-4 (P<0.01) and Vector (P<0.01), X61-4 was lower than that of the Vector (P<0.05). Conclusion:Cell experiment results show that lower ST6Gal I can effectively pro-mote the proliferation ability of SGC7901 gastric cancer cells, but high ST6Gal I can enhance gastric cancer cell migration ability. Therefore, ST6Gal I is related to the tumor proliferation and metastasis, and it is also a potential tumor molecular therapeutic targets.