Department of Otolaryngology, Xiangyang No. 1 People's Hospital, Hubei University of Medicine, Xiangyang, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1258-1263. doi: 10.26355/eurrev_202002_20180.
To investigate the effect of MiR-221 on proliferation and apoptosis of laryngeal carcinoma cells through the PI3K/AKT signaling pathway.
LipofectamineTM 2000 liposomes were used to transfer MiR-221 analogue, MiR-221 NC into Hep-2 cells of laryngeal carcinoma. Real-time fluorescence quantitative polymerase chain reaction (PCR) method was used to detect the expression of MiR-221, MTT method was used to detect the proliferation of cells, flow cytometry was used to detect cell cycle, Western blotting was used to detect the expression of apoptosis proteinase-1 (Apaf-1) and cyclin-dependent kinase (CDK1, CDK2) protein and the activation of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT).
Compared with MiR-221 NC group, the expression of MiR-221 in MiR-221 analogue group was up-regulated (p<0.01), the cell proliferation rate was decreased (p<0.01), the cell cycle was stagnated in the G1 phase (p<0.01), the expression levels of Cyclin A, CDK1, CDK2, PI3K, and p-AKT were significantly down-regulated (p<0.01), and the expression levels of Bax and Apaf-1 were significantly up-regulated (p<0.01).
MiR-221 analogues can significantly inhibit the proliferation and induce apoptosis of Hep-2 cells in laryngeal cancer, and this is achieved by blocking the PI3K/AKT signaling pathway, which also indicates that MiR-221 affects the proliferation and apoptosis of laryngeal cancer cells through the PI3K/AKT signaling pathway.
通过 PI3K/AKT 信号通路探讨 miR-221 对喉癌细胞增殖和凋亡的影响。
采用脂质体 2000 将 miR-221 类似物、miR-221 NC 转染入喉癌细胞 Hep-2 中，实时荧光定量聚合酶链反应（PCR）法检测 miR-221 的表达，MTT 法检测细胞增殖，流式细胞术检测细胞周期，Western blot 法检测凋亡蛋白酶-1（Apaf-1）和细胞周期蛋白依赖性激酶（CDK1、CDK2）蛋白的表达及磷酸肌醇 3 激酶（PI3K）/蛋白激酶 B（AKT）的活化。
与 miR-221 NC 组比较，miR-221 类似物组 miR-221 的表达上调（p<0.01），细胞增殖率下降（p<0.01），细胞周期停滞于 G1 期（p<0.01），Cyclin A、CDK1、CDK2、PI3K、p-AKT 表达水平显著下调（p<0.01），Bax、Apaf-1 表达水平显著上调（p<0.01）。
miR-221 类似物可显著抑制喉癌细胞 Hep-2 的增殖并诱导其凋亡，其作用机制可能是通过阻断 PI3K/AKT 信号通路实现的，这也表明 miR-221 可能通过 PI3K/AKT 信号通路影响喉癌细胞的增殖和凋亡。
