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首页|HOXA11-AS/miR-149-3p通路在肺鳞状细胞癌中的作用及机制研究

HOXA11-AS/miR-149-3p通路在肺鳞状细胞癌中的作用及机制研究

he role of HOXA11-AS/miR-149-3p pathway in the malignant phenotype of lung squamous cell carcinoma

中文摘要英文摘要

目的 探究长链非编码RNA HOXA11-AS在肺鳞状细胞癌发生过程中的确切机制。方法 采用定量聚合酶链式反应(RT-qPCR)检测HOXA11-AS、miR‐149-3p和SPT16表达变化。并通过MTT法检测细胞活力。双荧光素酶报告基因检测miR‐149-3p与HOXA11-AS或SPT16的互作关系。结果 在肺鳞状细胞癌组织和细胞中HOXA11-AS和SPT16的表达升高,而miR‐149-3p的表达降低。miR‐149-3p是HOXA11-AS的作用靶点,而SPT16是miR‐149-3p的作用靶点。HOXA11-AS的敲低抑制了肺鳞状细胞癌细胞的增殖能力,而使用miR‐149-3p抑制剂可拮抗HOXA11-AS敲低对肺鳞状细胞癌细胞增殖的抑制作用。此外,上调SPT16可减弱si-HOXA11-AS介导的肺鳞状细胞癌细胞的抗增殖作用。结论 HOXA11-AS的敲低可通过调控miR‐149-3p/SPT16轴在肺鳞状细胞癌中发挥抑癌作用。

Objective To explore the mechanism of long non-coding RNA HOXA11-AS in the carcinogenesis of lung squamous cell carcinoma. Methods The expression of HOXA11-AS, miR-149-3p and SPT16 was detected by quantitative polymerase chain reaction (RT-qPCR). The cell viability was detected by MTT method. Double luciferase reporter gene was used to detect the interaction between miR-149-3p and HOXA11-AS or SPT16. Results In lung squamous cell carcinoma, the expression of HOXA11-AS and SPT16 increased, while the expression of miR-149-3p decreased. MiR-149-3p is the target of HOXA11-AS, while SPT16 is the target of miR-149-3p. HOXA11-AS knockout inhibited the proliferation of lung squamous cell carcinoma cells, while the use of miR-149-3p inhibitor could antagonize the inhibitory effect of HOXA11-AS knockdown on the proliferation of lung squamous cell carcinoma cells. In addition, up-regulation of SPT16 can weaken the anti-proliferation effect of si-HOXA11-AS-mediated lung squamous cell carcinoma cells. Conclusion The knockdown of HOXA11-AS may play an inhibitory role in lung squamous cell carcinoma by regulating the miR-149-3p/SPT16 axis.

王红、赵静、唐秀花、黄珺霞

10.12201/bmr.202204.00005

肿瘤学基础医学分子生物学

肺鳞状细胞癌HOXA11-ASmiR-149-3p竞争性内源RNA

Lung squamous cell carcinomaHOXA11-ASmiR-149-3pcompetitive endogenous RNA

王红,赵静,唐秀花,黄珺霞.HOXA11-AS/miR-149-3p通路在肺鳞状细胞癌中的作用及机制研究[EB/OL].(2022-04-19)[2025-06-17].https://www.biomedrxiv.org.cn/article/doi/bmr.202204.00005.点此复制

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