翻译调控长非编码 RNA 1 通过 miR-22-3p/SP1 轴负向调节非小细胞肺癌细胞的放射敏感性。

IF 1.9 4区医学 Q3 RESPIRATORY SYSTEM

Clinical Respiratory Journal Pub Date : 2024-01-29 DOI:10.1111/crj.13734

Ming Zhong, Zheng Fang, Weixi Guo, Xiuyi Yu

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引用次数: 0

摘要

目标：非小细胞肺癌（NSCLC）占肺癌的 85%：非小细胞肺癌（NSCLC）占肺癌的 85%。长非编码 RNA（LncRNA）可调控癌症的放射敏感性。本研究探讨了lncRNA TRERNA1在NSCLC细胞放射敏感性中的作用机制：方法：测定NSCLC细胞系中LncRNA TRERNA1的水平。方法：测定 NSCLC 细胞系中 LncRNA TRERNA1 的水平，测量 NSCLC 细胞的辐射耐受性。分别在辐射耐受性最高/最低的 A549/HCC827 细胞中沉默或过表达 TRERNA1。检测了辐射诱导后 NSCLC 细胞中 γ-H2AX 和 SA-β-gal 的含量。通过双荧光素酶试验验证了 TRERNA1 与 miR-22-3p 的靶向结合以及 miR-22-3p 与 SP1 的靶向结合。检测到了 SP1 的表达。通过功能拯救实验证实了 miR-22-3p 和 SP1 在 TRERNA1 调控机制中的作用：结果：TRERNA1在NSCLC细胞中上调。沉默 TRERNA1 可增强 NSCLC 细胞的放射敏感性。沉默TRERNA1可提高辐射诱导后A549细胞中γ-H2AX和SA-β-gal的含量，而TRERNA1在HCC827细胞中的过表达则表现出相反的趋势。TRERNA1与miR-22-3p、miR-22-3p与SP1之间存在靶向关系，miR-22-3p抑制或SP1过表达可消除TRERNA1沉默的影响：结论：TRERNA1沉默通过miR-22-3p/SP1轴增强了NSCLC细胞的放射敏感性。这项研究可能为治疗 NSCLC 提供新的靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Translation regulatory long non-coding RNA 1 negatively regulates cell radiosensitivity via the miR-22-3p/SP1 axis in non-small cell lung cancer

查看原文本刊更多论文

Translation regulatory long non-coding RNA 1 negatively regulates cell radiosensitivity via the miR-22-3p/SP1 axis in non-small cell lung cancer

Objective

Non-small cell lung cancer (NSCLC) occupies 85% of lung cancer. Long non-coding RNAs (LncRNAs) can regulate the radiosensitivity of cancers. This study explored the mechanism of lncRNA TRERNA1 in the radiosensitivity of NSCLC cells.

Methods

LncRNA TRERNA1 level in NSCLC cell lines was determined. NSCLC cell radiation tolerance was measured. TRERNA1 expression was silenced or overexpressed in A549/HCC827 cells with the highest/lowest radiation tolerance, respectively. The contents of γ-H2AX and SA-β-gal in NSCLC cells after radiation induction were detected. The targeted binding of TRERNA1 to miR-22-3p and miR-22-3p to SP1 were verified by dual-luciferase assay. SP1 expression were detected. Functional rescue experiments were implemented to confirm the roles of miR-22-3p and SP1 in the regulatory mechanism of TRERNA1.

Results

TRERNA1 was upregulated in NSCLC cells. TRERNA1 silencing enhanced radiosensitivity of NSCLC cells. TRERNA1 silencing elevated the contents of γ-H2AX and SA-β-gal in A549 cells after radiation induction, while TRERNA1 overexpression showed an opposite trend in HCC827 cells. There were targeting relationships between TRERNA1 and miR-22-3p, and miR-22-3p and SP1. miR-22-3p repression or SP1 overexpression abolished the effects of TRERNA1 silencing.

Conclusion

TRERNA1 silencing enhanced radiosensitivity of NSCLC cells via the miR-22-3p/SP1 axis. This study may offer new targets for NSCLC treatment.

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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)