miR-625-5p通过靶向调控PRKACA促进肺腺癌细胞的增殖和侵袭

背景 与目的:肺腺癌是非小细胞肺癌的一种亚型,虽在诊断和治疗方面已经取得了很大进展,但晚期肺腺癌临床预后和总生存仍较差.近年来多项研究表明,miRNA在多种癌症中发挥作用,并在细胞增殖、转移、炎症等生物学过程中发挥重要作用.探究miR-625-5p对肺腺癌细胞增殖和侵袭能力的影响及分子机制,旨在为后续肺腺癌的诊断和治疗...

miR-625-5p promotes proliferation and invasion of lung adenocarcinoma by targeting PRKACA

Background and purpose: Lung adenocarcinoma is a subtype of non-small cell lung cancer. Although much progress has been made in the diagnosis and treatment of lung adenocarcinoma, the clinical prognosis and overall survival of advanced lungadenocarcinoma are still poor. In recent years, a number of studies have shown that miRNA can play a role in a variety of cancers, and play an important role in cell proliferation, metastasis, inflammation and other biological processes. This study aimed to explore the effect of miR-625-5p on the proliferation and invasion ability of lung adenocarcinoma cells and its molecular mechanism, so as to provide a new idea for the diagnosis and treatment of lung cancer. Methods: GEO database was used to search for differentially expressed miRNA in lung adenocarcinoma. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of miR-625-5p in various lung adenocarcinoma cell lines. The effects of miR-625-5p on the proliferation and invasion of lung adenocarcinoma cells were investigated by EdU cell proliferation assay and transwell invasion assay. Key genes of miR-625-5p targeted binding were predicted by bioinformatics. Western blot experiment validated the expression of protein kinase cAMP-activated catalytic subunit alpha (PRKACA) in lung adenocarcinoma cells. The targeted relationship between miR-625-5p and PRKACA was analyzed by double luciferase assay and Western blot. Western blot assay was used to detect the expression of PRKACA after co-transfection of si-PRKACA and si-miR-625-5p in each group. The effect of miR-625-5p on the proliferation and invasion ability of lung adenocarcinoma cells by targeting PRKACA was observed by EdU cell proliferation assay and transwell invasion assay. Results: The expression of miR-625-5p was up-regulated in lung adenocarcinoma tissues (P<0.000 1) and cells (P<0.000 1). The results of EdU cell proliferation assay and transwell invasion assay showed that miR-625-5p promoted the proliferation (P=0.002 3) and invasion (P=0.000 3) of lung adenocarcinoma cells. Double luciferase assay showed that miR-625-5p could target and bind to PRKACA (P=0.000 8). In lung adenocarcinoma cells, miR-625-5p was negatively correlated with PRKACA expression (P<0.000 1). Down-regulation of miR-625-5p reversed the promotion of the proliferation (P=0.011 9) and invasion (P=0.001 5) ability of A549 cells by knockout of PRKACA. Conclusion: MiR-625-5p is up-regulated in lung adenocarcinoma and promotes proliferation and invasion of lung adenocarcinoma tissues and cells by negatively regulating PRKACA.