ITGB1-DT/ARNTL2 axis may be a novel biomarker in lung adenocarcinoma: a bioinformatics analysis and experimental validation.

ITGB1-DT/ARNTL2 axis may be a novel biomarker in lung adenocarcinoma: a bioinformatics analysis and experimental validation.
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ITGB1-DT/ARNTL2轴可能是肺腺癌的新型生物标志物:生物信息学分析和实验验证

DOI:
10.1186/s12935-021-02380-2
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发表时间:
2021-12-14
影响因子:
5.8
通讯作者:
Wu YB
Wu YB
中科院分区:
医学2区
文献类型:
--
作者:
Qiu BQ;Lin XH;Lai SQ;Lu F;Lin K;Long X;Zhu SQ;Zou HX;Xu JJ;Liu JC;Wu YB

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肺癌是危害人类健康最致命的恶性肿瘤之一。近几十年来,肺腺癌 (LUAD) 急剧增加,占所有肺癌病例的近 40%。越来越多的证据表明竞争性内源性 RNA (ceRNA) 内在机制在各种人类癌症中的重要性。然而,肺腺癌中ceRNA网络的行为特征需要进一步研究。本研究使用基于 SLC2A1 表达的分组来识别肺腺癌中的相关 ceRNA 网络和潜在预后标志物。癌症基因组图谱(TCGA)数据库用于获取患者的lncRNA、miRNA和mRNA表达谱以及临床数据。采用信息学技术研究hub基因对预后的影响。进行 Cox 回归分析以评估 hub 基因的预后效果。利用甲基化、GSEA 和免疫浸润分析来探索 hub 基因的潜在机制。采用CCK-8、Transwell、集落形成实验检测肺癌细胞的增殖和侵袭能力。我们最终确定 ITGB1-DT/ARNTL2 轴是一个可能促进肺腺癌进展的独立事实。此外,甲基化分析显示低甲基化可能导致ITGB1-DT/ARNTL2轴失调,免疫浸润分析显示ITGB1-DT/ARNTL2轴可能影响免疫微环境和肺腺癌的进展。 CCK-8、transwell 和结肠形成测定表明 ITGB1-DT/ARNTL2 促进肺腺癌的进展。 hsa-miR-30b-3p 逆转了 ITGB1/ARNTL2 介导的致癌过程。我们的研究发现 ITGB1-DT/ARNTL2 轴是一种影响肺腺癌预后的新型预后生物标志物。在线版本包含可在 10.1186/s12935-021-02380-2 获取的补充材料。
Lung cancer is one of the most lethal malignant tumors that endangers human health. Lung adenocarcinoma (LUAD) has increased dramatically in recent decades, accounting for nearly 40% of all lung cancer cases. Increasing evidence points to the importance of the competitive endogenous RNA (ceRNA) intrinsic mechanism in various human cancers. However, behavioral characteristics of the ceRNA network in lung adenocarcinoma need further study. Groups based on SLC2A1 expression were used in this study to identify associated ceRNA networks and potential prognostic markers in lung adenocarcinoma. The Cancer Genome Atlas (TCGA) database was used to obtain the patients' lncRNA, miRNA, and mRNA expression profiles, as well as clinical data. Informatics techniques were used to investigate the effect of hub genes on prognosis. The Cox regression analyses were performed to evaluate the prognostic effect of hub genes. The methylation, GSEA, and immune infiltration analyses were utilized to explore the potential mechanisms of the hub gene. The CCK-8, transwell, and colony formation assays were performed to detect the proliferation and invasion of lung cancer cells. We eventually identified the ITGB1-DT/ARNTL2 axis as an independent fact may promote lung adenocarcinoma progression. Furthermore, methylation analysis revealed that hypo-methylation may cause the dysregulated ITGB1-DT/ARNTL2 axis, and immune infiltration analysis revealed that the ITGB1-DT/ARNTL2 axis may affect the immune microenvironment and the progression of lung adenocarcinoma. The CCK-8, transwell, and colonu formation assays suggested that ITGB1-DT/ARNTL2 promotes the progression of lung adenocarcinoma. And hsa-miR-30b-3p reversed the ITGB1/ARNTL2-mediated oncogenic processes. Our study identified the ITGB1-DT/ARNTL2 axis as a novel prognostic biomarker affects the prognosis of lung adenocarcinoma. The online version contains supplementary material available at 10.1186/s12935-021-02380-2.