Circular RNA NFIX Functions as an Oncogene in Non-Small Cell Lung Cancer by Modulating the miR-214-3p/TRIAP1 Axis

IF 1.9 4区医学 Q3 RESPIRATORY SYSTEM Clinical Respiratory Journal Pub Date : 2024-08-12 DOI:10.1111/crj.13801

Guohua Liu, Hanbing Shi, Hongyan Zheng, Weili Kong, Xinyue Cheng, Liling Deng

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Abstract

Background

circRNA NFIX has been shown to exist as an oncogene in glioma. But its expression and role in NSCLC (non-small cell lung cancer) are still unclear. This research aimed to discover the expression and function of circRNA NFIX in NSCLC.

Methods

In this research, qRT-PCR was utilized to investigate the expression levels of circRNA NFIX, miRNA-214-3p, and TRIAP1 in NSCLC tissues and cell lines. The binding sites between circRNA NFIX/TRIAP1 and miRNA-214-3p were predicted using the Starbase. These interactions were further validated using a double luciferase reporter assay. Cell proliferation and apoptosis were assessed through MTT and flow cytometry, respectively. The expression of apoptosis-related proteins was measured by western blot assay.

Results

miRNA-214-3p could link with circRNA NFIX. circRNA NFIX was upregulated, while miRNA-214-3p was downregulated in NSCLC cell lines and clinical samples. Besides, suppression of circRNA NFIX repressed cell proliferation and induced apoptosis in NSCLC cells by upregulating miRNA-214-3p expression. Besides, the data indicated that TRIAP1 was a target of miRNA-214-3p, and it was negatively regulated by miRNA-214-3p in NSCLC cells. The excessive expression of miRNA-214-3p suppressed NSCLC cell proliferation and increased apoptosis. In addition, overexpression of TRIAP1 significantly reversed the effects on NSCLC cells caused by miRNA-214-3p mimic.

Conclusion

circRNA NFIX silencing repressed the proliferation of NSCLC cells and induced cell apoptosis by regulating the miR-214-3p/TRIAP1 axis, which was a potential diagnostic and therapeutic target for NSCLC.

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环状 RNA NFIX 通过调节 miR-214-3p/TRIAP1 轴在非小细胞肺癌中发挥癌基因的功能

背景：circRNA NFIX 已被证明是胶质瘤的致癌基因。但它在 NSCLC（非小细胞肺癌）中的表达和作用仍不清楚。本研究旨在发现 circRNA NFIX 在 NSCLC 中的表达和功能：方法：本研究利用 qRT-PCR 技术检测了 circRNA NFIX、miRNA-214-3p 和 TRIAP1 在 NSCLC 组织和细胞系中的表达水平。利用Starbase预测了circRNA NFIX/TRIAP1与miRNA-214-3p之间的结合位点。使用双荧光素酶报告实验进一步验证了这些相互作用。细胞增殖和凋亡分别通过 MTT 和流式细胞术进行评估。结果表明：miRNA-214-3p 可与 circRNA NFIX 连接。在 NSCLC 细胞系和临床样本中，circRNA NFIX 上调，而 miRNA-214-3p 下调。此外，抑制 circRNA NFIX 可抑制细胞增殖，并通过上调 miRNA-214-3p 的表达诱导 NSCLC 细胞凋亡。此外，数据还表明，TRIAP1是miRNA-214-3p的靶标，它在NSCLC细胞中受到miRNA-214-3p的负调控。miRNA-214-3p的过度表达抑制了NSCLC细胞的增殖，增加了细胞的凋亡。结论：circRNA NFIX沉默通过调节miR-214-3p/TRIAP1轴抑制NSCLC细胞增殖并诱导细胞凋亡，是NSCLC的潜在诊断和治疗靶点。

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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来源期刊

Clinical Respiratory Journal 医学-呼吸系统

CiteScore

3.70

自引率

0.00%

发文量

104

审稿时长

>12 weeks

期刊介绍： Overview Effective with the 2016 volume, this journal will be published in an online-only format. Aims and Scope The Clinical Respiratory Journal (CRJ) provides a forum for clinical research in all areas of respiratory medicine from clinical lung disease to basic research relevant to the clinic. We publish original research, review articles, case studies, editorials and book reviews in all areas of clinical lung disease including: Asthma Allergy COPD Non-invasive ventilation Sleep related breathing disorders Interstitial lung diseases Lung cancer Clinical genetics Rhinitis Airway and lung infection Epidemiology Pediatrics CRJ provides a fast-track service for selected Phase II and Phase III trial studies. Keywords Clinical Respiratory Journal, respiratory, pulmonary, medicine, clinical, lung disease, Abstracting and Indexing Information Academic Search (EBSCO Publishing) Academic Search Alumni Edition (EBSCO Publishing) Embase (Elsevier) Health & Medical Collection (ProQuest) Health Research Premium Collection (ProQuest) HEED: Health Economic Evaluations Database (Wiley-Blackwell) Hospital Premium Collection (ProQuest) Journal Citation Reports/Science Edition (Clarivate Analytics) MEDLINE/PubMed (NLM) ProQuest Central (ProQuest) Science Citation Index Expanded (Clarivate Analytics) SCOPUS (Elsevier)