摘要
目的探讨在两株胃癌细胞株BGC-823及SGC-7901中抑制内源性miR-24的表达后对细胞凋亡和增殖的作用。方法使用INTERFERin转染试剂将锁核苷酸标记的反义核酸miR-24-ASO转染进入胃癌细胞株,使用倒置荧光显微镜观察细胞生长变化,流式细胞计检测细胞凋亡的比例,然后使用CCK-8试剂盒对细胞增殖情况进行检测。结果转染miR-24-ASO的BGC-803细胞和SGC-7901细胞相对于转染内参的凋亡水平分别增加了约2.5倍和2.1倍左右。转染了miR-24-ASO抑制内源性miR-24的表达之后细胞的增殖能力相对于转染阴性对照的细胞株的增殖能力均明显降低。结论抑制内源性miR-24的表达可以诱导胃癌细胞的凋亡并导致胃癌细胞增殖能力的降低。miR-24调控了胃癌细胞的增殖和凋亡过程。揭示了miRNA在胃癌发生过程中的调控机制,并为胃癌的治疗提供了良好的应用前景。
Objective To Explore the two cancer line BGC -803 and SGC -7901 in the inhibition of endogenous miR - 24 after the expression of apoptosis and proliferation. Methods miR - 24 - ASO was transfected into BGC - 803 and SGC - 7901 cells with transfection agent to down - regulate the expression of endogenous miR - 24. The cellular growth activity was assayed by CCK - 8 kit, and the apoptosis was tested by flow cytometry. Results The apoptosis rates of BGC - 803 and SGC - 7901 cells transfected with miR - 24 - ASO were about 2. 5 and 2. 1 times more than which transfected with nega- tive control NC - ASO. The ability of proliferation of BGC - 803 and SGC - 7901 ceils was greatly reduced after miR - 24 was down - regulated by miR - 24 - ASO. Conclusion The miR - 24 down - regulation can suppress the cellular proliferation and induce apoptosis in BGC -803 and SGC -7901 cells, miR -24 regulates cell proliferation and apoptosis in gastric cancer cells. And it may have a strong rationale for therapeutic applications in gastric cancer in the future.
出处
《中国医学创新》
CAS
2011年第13期1-4,共4页
Medical Innovation of China
基金
973项目(2005CB724602)
中科院重要方向性项目(KSCX-2-SW-228和KSCX1-YW-R-64)
