TMEM176B调控乳腺癌凋亡作用及机制研究
The Mechanism of TMEM176B in Apoptosis of Breast Cancer
DOI: 10.12677/WJCR.2019.93012, PDF,   
作者: 杨 翀:广州卫生职业技术学院,广东 广州;苏宝倡*:暨南大学附属华侨医院,广东 广州
关键词: 乳腺癌TMEM176BBcl-2BaxKi67p53和p-AKT信号通路Breast Cancer TMEM176B Bcl-2 Bax Ki67 P53 and P-AKT Signaling Pathways
摘要: 目的:研究跨膜蛋白176B (Transmembrane protein 176B, TMEM176B)在乳腺癌中凋亡作用及机制。方法:qRT-PCR、western blot法检测乳腺癌组织中TMEM176B表达;小分子干扰RNA和干扰TMEM176B后研究其作用和分子机制。MTT法和CCK8实验检测乳腺癌细胞生长情况;流式细胞实验检测乳腺癌凋亡作用。结果:干扰TMEM176B后明显抑制乳腺癌活力和诱导乳腺癌凋亡,抑制细胞增殖蛋白Ki67表达,且下调抑凋亡蛋白Bcl-2和上调促凋亡蛋白Bax表达水平。在机制方面,我们发现干扰TMEM176B后下调p53表达和p-AKT水平。结论:TMEM176B通过调控p53表达和p-AKT水平进而调控乳腺癌凋亡作用。
Abstract: Objective: To study the role and mechanism of transmembrane protein 176B (TMEM176B) in breast cancer. Methods: The expression of TMEM176B in breast cancer tissue was detected by qRT-PCR and Western blot, and using small interfering RNA for silencing TMEM176B level. MTT assay and CCK8 assay were used to detect the viability of breast cancer cells, and flow cytometry was used to detect the apoptosis of breast cancer cells. Results: Small interfering RNA significantly knocked down the level of TMEM176B, inhibited the growth of breast cancer. In terms of mechanism, siRNA inhibited the cell proliferation protein Ki67 expression, and down-regulated the expression of apoptotic protein Bcl-2 and up-regulated the expression of apoptotic protein Bax. Furthermore, the result showed that the expression of p53 and the level of p-AKT were down-regulated after TMEM176B interference. Conclusion: knockdown of TMEM176B promotes the apoptosis of breast cancer by regulating the expression of p53 and the level of p-AKT.
文章引用:杨翀, 苏宝倡. TMEM176B调控乳腺癌凋亡作用及机制研究[J]. 世界肿瘤研究, 2019, 9(3): 82-89. https://doi.org/10.12677/WJCR.2019.93012

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