CircSEC24A induces KLF8 expression to promote the malignant progression of non-small cell lung cancer by regulating miR-1253.

IF 2.3 3区医学 Q3 ONCOLOGY Thoracic Cancer Pub Date : 2024-10-28 DOI:10.1111/1759-7714.15450

Wei Xiong, Jinhua Yang

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Abstract

Objectives: This study aimed to analyze the role of circSEC24A in non-small cell lung cancer (NSCLC) and its underlying mechanism.

Methods: RNA levels of circSEC24A, microRNA-1253 (miR-1253), and KLF transcription factor 8 (KLF8) were detected by quantitative real-time polymerase chain reaction. Protein expression was analyzed by western blot or immunohistochemistry assay. Cell proliferation and apoptosis were investigated by colony formation assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry analysis. Glycolysis was evaluated by commercial kits. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to identify the associations among circSEC24A, miR-1253, and KLF8. Xenograft mouse model assay was used to evaluate the effect of circSEC24A on tumor tumorigenesis.

Results: CircSEC24A and KLF8 were upregulated, while miR-1253 was downregulated in NSCLC. CircSEC24A knockdown inhibited proliferation and glycolysis but induced the apoptosis of NSCLC cells. CircSEC24A acted as a miR-1253 sponge and regulated NSCLC cell malignancy by targeting miR-1253. KLF8 was identified as a target of miR-1253, and its overexpression attenuated miR-1253-induced effects in NSCLC cells. Besides, circSEC24A upregulated KLF8 by sponging miR-1253. Further, circSEC24A knockdown suppressed NSCLC cell tumorigenesis in vivo.

Conclusions: CircSEC24A silencing inhibited NSCLC cell malignancy through the miR-1253/KLF8 pathway, providing a potential therapeutic target for NSCLC.

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CircSEC24A通过调控miR-1253诱导KLF8的表达，从而促进非小细胞肺癌的恶性进展。

研究目的本研究旨在分析circSEC24A在非小细胞肺癌（NSCLC）中的作用及其内在机制：方法：采用实时定量聚合酶链反应检测circSEC24A、microRNA-1253（miR-1253）和KLF转录因子8（KLF8）的RNA水平。蛋白表达通过 Western 印迹或免疫组化检测进行分析。细胞增殖和凋亡通过菌落形成检测、5-乙炔基-2'-脱氧尿苷检测和流式细胞仪分析进行研究。糖酵解采用商业试剂盒进行评估。通过双荧光素酶报告实验和 RNA 免疫沉淀实验来确定 circSEC24A、miR-1253 和 KLF8 之间的关联。采用异种移植小鼠模型试验评估 circSEC24A 对肿瘤发生的影响：结果：CircSEC24A和KLF8在NSCLC中上调，而miR-1253下调。敲除 CircSEC24A 可抑制 NSCLC 细胞的增殖和糖酵解，但可诱导其凋亡。CircSEC24A作为miR-1253的海绵，通过靶向miR-1253调控NSCLC细胞的恶性程度。KLF8被鉴定为miR-1253的靶标，其过表达可减轻miR-1253诱导的NSCLC细胞效应。此外，circSEC24A通过疏导miR-1253而上调KLF8。此外，circSEC24A敲除抑制了NSCLC细胞在体内的肿瘤发生：结论：沉默circSEC24A可通过miR-1253/KLF8途径抑制NSCLC细胞的恶性生长，为NSCLC提供了一个潜在的治疗靶点。

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

Thoracic Cancer ONCOLOGY-RESPIRATORY SYSTEM

CiteScore

5.20

自引率

3.40%

发文量

439

审稿时长

2 months

期刊介绍： Thoracic Cancer aims to facilitate international collaboration and exchange of comprehensive and cutting-edge information on basic, translational, and applied clinical research in lung cancer, esophageal cancer, mediastinal cancer, breast cancer and other thoracic malignancies. Prevention, treatment and research relevant to Asia-Pacific is a focus area, but submissions from all regions are welcomed. The editors encourage contributions relevant to prevention, general thoracic surgery, medical oncology, radiology, radiation medicine, pathology, basic cancer research, as well as epidemiological and translational studies in thoracic cancer. Thoracic Cancer is the official publication of the Chinese Society of Lung Cancer, International Chinese Society of Thoracic Surgery and is endorsed by the Korean Association for the Study of Lung Cancer and the Hong Kong Cancer Therapy Society. The Journal publishes a range of article types including: Editorials, Invited Reviews, Mini Reviews, Original Articles, Clinical Guidelines, Technological Notes, Imaging in thoracic cancer, Meeting Reports, Case Reports, Letters to the Editor, Commentaries, and Brief Reports.