CAJ | 학술논문

目的：研究 miR-98对肝癌 HepG2细胞增殖、凋亡和侵袭、迁移能力的影响及其可能机制。方法将 miR-98mimics、mimics-NC、miR-98inhibitor、inhibitor-NC 瞬时转入肝癌 HepG2细胞内,应用噻唑盐( MTT)法、流式细胞仪、Tr-answell 小室实验检测 miR-98对肝癌 HepG2细胞增殖、凋亡以及侵袭、迁移能力的影响,进一步用 Western blot 法检测各组 Bcl-2蛋白的表达水平。结果 MTT 实验表明 miR-98过表达后,肝癌细胞的增殖能力明显低于对照组；Annexin V-FITC / PI 凋亡实验证实上调 miR-98表达后,细胞的凋亡率较对照组升高；Transwell 小室实验表明上调 miR-98可使肝癌细胞的侵袭、迁移能力减弱。而当 miR-98被抑制后,肝癌HepG2细胞的增殖及侵袭、迁移能力则明显增强,凋亡率则下降。 Western blot 实验检测发现 miR-98过表达后,Bcl-2的表达降低。结论 miR-98可能在肝癌的发生、发展中发挥着抑癌基因的作用；miR-98可能通过下调 Bcl-2的表达,促进肝癌 HepG2细胞凋亡。
목적：연구 miR-98대간암 HepG2세포증식、조망화침습、천이능력적영향급기가능궤제。방법장 miR-98mimics、mimics-NC、miR-98inhibitor、inhibitor-NC 순시전입간암 HepG2세포내,응용새서염( MTT)법、류식세포의、Tr-answell 소실실험검측 miR-98대간암 HepG2세포증식、조망이급침습、천이능력적영향,진일보용 Western blot 법검측각조 Bcl-2단백적표체수평。결과 MTT 실험표명 miR-98과표체후,간암세포적증식능력명현저우대조조；Annexin V-FITC / PI 조망실험증실상조 miR-98표체후,세포적조망솔교대조조승고；Transwell 소실실험표명상조 miR-98가사간암세포적침습、천이능력감약。이당 miR-98피억제후,간암HepG2세포적증식급침습、천이능력칙명현증강,조망솔칙하강。 Western blot 실험검측발현 miR-98과표체후,Bcl-2적표체강저。결론 miR-98가능재간암적발생、발전중발휘착억암기인적작용；miR-98가능통과하조 Bcl-2적표체,촉진간암 HepG2세포조망。
Objective To investigate the potential mechanism of miR-98’s effects on proliferation, apoptosis, and invasion / migration of HepG2 hepatocellular carcinoma (HCC) cells. Methods miR-98mimics, mimics-NC, miR-98 inhibitor and inhibitor-NC were transiently transfected into HepG2 cells. Effects of miR-98 on proliferation,ap-optosis, invasion / migration of HepG2 cells were determined by MTT assay, flow cytometer, and Transwell assay. Western blot was then performed to determine Bcl-2 expression levels in each group. Results MTT assay demon-strated that proliferation rate of HepG2 cells in miR-98 overexpressing group was significantly lower compared with control groups. Annexin V-FITC / PI revealed that apoptosis was more prominent in miR-98 overexpressing group compared with control groups. Transwell assay revealed that invasion and migration were significantly attenuated in miR-98 overexpressing group compared with control groups. Western blot demonstrated that Bcl-2 expression level was lower in miR-98 overexpression group compared with control groups. Conclusion miR-98 serves as a suppres-sor in the development of HCC; miR-98 promotes apoptosis of HCC cells by down regulating expression of Bcl-2.