[COL11A1 regulates PI3K/Akt/GSK-3β pathway and promotes human lung adenocarcinoma primary cell migration and invasion].

S Y Yang, L H Zhu, R Yang, T T Liao, X W Hu
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引用次数: 0

Abstract

Objective: To investigate the role and mechanism of COL11A1 in lung adenocarcinoma migration and invasion. Methods: Surgical pathological tissues of 4 patients with lung adenocarcinoma admitted to the Affiliated Hospital of Guizhou Medical University from September to November 2020 were used. Immunohistochemical methods were used to identify lung adenocarcinoma tissues, para-cancerous tissues and parallel transcriptome sequencing. Genetic prognostic analysis was conducted by TCGA and GTEx databases.The expression level of COL11A1 gene in lung adenocarcinoma and adjacent tissues was detected by Western blotting.The primary human lung adenocarcinoma cells cultured. The COL11A1 siRNA was transfected into primary human lung adenocarcinoma cells, then the transcriptome sequencing of differential genes was performed,and KEGG enrichment analysis of differential gene enrichment pathway was conducted. Protein expression and phosphorylation were detected by Western blot method. Cell migration was detected by scratch healing test. Cell proliferation was detected by CCK8 method and invasion ability was detected by Transwell method. Results: Ten differentially expressed genes were screened by transcription sequencing in lung adenocarcinoma. Prognostic analysis of single gene showed that COL11A1 gene expression level was correlated with survival rate (P<0.001). The expression of COL11A1 in lung adenocarcinoma was higher than that in adjacent tissues by Western blot (P<0.001). Transcriptome sequencing of COL11A1 siRNA transfection into primary human lung adenocarcinoma cells showed that differential genes were concentrated in PI3K-akt pathway. The expression of tumor suppressor gene PTEN in siRNA transfection group was significantly higher than that in control group and negative transfection group by Western blot. The expression of Aktp-Akt 473 p-Akt 308 p-PTENp-PDK1p-c-Rafp-GSK-3 β was down-regulated (all P<0.05).Compared with the negative control group, the ability of migration, proliferation and invasion of primary human lung adenocarcinoma cells in siRNA transfection group decreased (all P<0.05). COL11A1 regulates PI3K/Akt/GSK-3 β pathway to promote migration and invasion of primary human lung adenocarcinoma cells. Conclusion: COL11A1 regulates PI3K/Akt/GSK-3 β pathway to promote migration and invasion of primary human lung adenocarcinoma cells.

[COL11A1调节PI3K/Akt/GSK-3β通路,促进人肺腺癌原代细胞迁移和侵袭]。
目的:探讨COL11A1在肺腺癌迁移侵袭中的作用及机制。方法:选取2020年9月至11月贵州医科大学附属医院收治的4例肺腺癌患者的手术病理组织。采用免疫组化方法鉴定肺腺癌组织和癌旁组织,并进行平行转录组测序。采用TCGA和GTEx数据库进行遗传预后分析。Western blotting检测COL11A1基因在肺腺癌及癌旁组织中的表达水平。原代人肺腺癌细胞的培养。将COL11A1 siRNA转染原代人肺腺癌细胞,对差异基因进行转录组测序,并对差异基因富集途径进行KEGG富集分析。Western blot法检测蛋白表达和磷酸化水平。用划痕愈合试验检测细胞迁移。CCK8法检测细胞增殖,Transwell法检测细胞侵袭能力。结果:通过转录测序筛选出肺腺癌组织中10个差异表达基因。结论:COL11A1通过调控PI3K/Akt/GSK-3 β通路促进原发性人肺腺癌细胞的迁移和侵袭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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