Department of Gynaecology, Funing People's Hospital, Yancheng City, JiangSu Province, China.
Bioengineered. 2021 Dec;12(2):10596-10607. doi: 10.1080/21655979.2021.2000722.
To probe into the potential mechanism of microRNA (miR)-98-5p inhibiting the biological progress of cervical cancer (CC) cells via regulating PI3K/Akt pathway. Reverse transcription quantitative polymerase chain reaction was applied to detect miR-98-5p expression in CC tissues and cell lines; Cell counting kit-8 and Edu analysis were performed for checking cell proliferation, flow cytometry for cell apoptosis, transwell for cell invasion and migration, Western blot for proliferation-related proteins Ki67 and Proliferating cell nuclear antigen expression, apoptosis-related proteins Bcl-2 and Bax expression, epithelial-mesenchymal transition (EMT)-related proteins Snail, matrix metalloproteinase-3, E-cadherin and N-cadherin expression, as well as PI3K/Akt pathway-related proteins PTEN, PI3K as well as Akt expression levels, and the nude mouse tumor xenograft experiment was applied to verify . The result clarified, miR-98-5p was reduced in CC. Overexpression miR-98-5p could inhibit CC cell proliferation, invasion, migration and EMT, whereas promoted its apoptosis, but silencing miR-98-5p was opposite. Overexpression miR-98-5p could depress the activation of PI3K/Akt pathway in CC and . MiR-98-5p targeted CBX5. In short, miR-98-5p is able to be used as a potential target for treating CC in future research.
探讨 microRNA(miR)-98-5p 通过调控 PI3K/Akt 通路抑制宫颈癌(CC)细胞生物学进展的潜在机制。采用逆转录定量聚合酶链反应检测 CC 组织和细胞系中 miR-98-5p 的表达;细胞计数试剂盒-8 和 Edu 分析检测细胞增殖,流式细胞术检测细胞凋亡,Transwell 检测细胞侵袭和迁移,Western blot 检测增殖相关蛋白 Ki67 和增殖细胞核抗原表达,凋亡相关蛋白 Bcl-2 和 Bax 表达,上皮-间充质转化(EMT)相关蛋白 Snail、基质金属蛋白酶-3、E-钙黏蛋白和 N-钙黏蛋白表达,以及 PI3K/Akt 通路相关蛋白 PTEN、PI3K 和 Akt 表达水平,并应用裸鼠肿瘤移植实验进行验证。结果表明,miR-98-5p 在 CC 中表达降低。过表达 miR-98-5p 可抑制 CC 细胞增殖、侵袭、迁移和 EMT,促进其凋亡,而沉默 miR-98-5p 则相反。过表达 miR-98-5p 可抑制 CC 中 PI3K/Akt 通路的激活。miR-98-5p 靶向 CBX5。总之,miR-98-5p 可作为未来研究中治疗 CC 的潜在靶点。