MiR-15b mediates liver cancer cells proliferation through targeting BCL-2

被引:2
|
作者
Zhang, Yuping [1 ]
Huang, Feizhou [1 ]
Wang, Jian [2 ]
Peng, Lin [2 ]
Luo, Hongwu [1 ]
机构
[1] Cent S Univ, Xiangya Hosp 3, Dept Gen Surg, 138 Tongzipo Rd, Changsha 410000, Hunan, Peoples R China
[2] Genet Res Lab CSU, Changsha 410000, Hunan, Peoples R China
关键词
Liver cancer; miR-15b; BCL2; proliferation; HEPATOCELLULAR-CARCINOMA; LUNG-CANCER; EXPRESSION; TRIPTOLIDE; MICRORNAS; THERAPY; COMBINATION; MIRNAS; GENES; RISK;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The incidence and mortality of liver cancer increased year by year. Our country presents high incidence of liver cancer. MicroRNAs have tissue sensitivity as tumor biomarkers that play a role by promoting tumor growth as oncogenes or inhibit malignant cell growth as tumor suppressor genes. Studies showed that miR-15b abnormal expression in the tumor and can be treated as one of the tumor molecular markers. However, miR-15b expression and role in the liver cancer cells have not been elucidated. This study intended to explore the mechanism of miR-15b effect on liver cancer occurrence and development. Liver cancer cell line HepG2 was transfected with miR-15b mimic or inhibitor. Real-time PCR was applied to detect miR-15b expression. MTT was used to test cell proliferation. Transwell assay was performed to determine cell invasive ability. Real-time PCR and Western blot were used to detect BCL2 expression. MiR-15b mimic transfection promoted miR-15b overexpression and inhibited HepG2 cell proliferation significantly (P < 0.05). MiR-15b overexpression downregulated BCL2 mRNA and protein expression obviously (P < 0.05). On the contrary, miR-15b inhibitor transfection markedly reduced miR-15b expression in liver cancer cells (P < 0.05), promoted tumor cell proliferation, and increased BCL2 mRNA and protein expression. MiR-15b expression changes did not affect cell invasion (P > 0.05). MiR-15b can inhibit HepG2 cell proliferation and down-regulate BCL2 mRNA and protein expression.
引用
收藏
页码:15677 / 15683
页数:7
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