HNRNPH1 promotes autophagy to inhibit the development of lung adenocarcinoma via the HSP90AB1/MAP1LC3B axis.

IF 5.8 2区医学 Q1 Medicine

Respiratory Research Pub Date : 2025-06-04 DOI:10.1186/s12931-025-03280-z

Rong Li, Fen Li, Qian Liu, Xu Wu, Xiaowu Tan

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引用次数: 0

Abstract

Background: Lung adenocarcinoma (LUAD) is a prevalent subtype of lung cancer (LC) whose progression is regulated by multiple genes. This study sought to find the impact and mechanism of HNRNPH1 on LUAD.

Methods: The expression and role of HSP90AB1, HNRNPH1, and autophagy-related protein MAP1LC3B in LUAD were detected. Additionally, bioinformatics analysis, silencing and overexpression techniques, and in vivo modeling were used to explore the regulatory mechanisms of these proteins in the progression of LUAD.

Results: HSP90AB1 showed high expression in LUAD and was linked to a worse prognosis. Overexpression of HSP90AB1 significantly promoted the malignant phenotype of LUAD cells and inhibited MAP1LC3B-mediated autophagy. However, overexpression of HNRNPH1 could reverse the malignant phenotype resulting from HSP90AB1 overexpression and promote MAP1LC3B-mediated autophagy by binding to HSP90AB1 mRNA and inhibiting its protein expression. Animal experiments also revealed that overexpression of HNRNPH1 could inhibit tumor progression by promoting cellular autophagy.

Conclusions: We verified the key role of HSP90AB1, HNRNPH1, and MAP1LC3B in LUAD, and revealed a possible regulatory mechanism, namely, HNRNPH1 could inhibit the development of LUAD by promoting autophagy through the HSP90AB1/MAP1LC3B axis. These findings may offer new insights for improving the treatment and prognosis of LUAD.

Clinical trial number: Not applicable.

查看原文本刊更多论文

HNRNPH1通过HSP90AB1/MAP1LC3B轴促进自噬抑制肺腺癌的发展。

背景：肺腺癌（LUAD）是肺癌（LC）的一种常见亚型，其进展受多种基因调控。本研究旨在发现HNRNPH1对LUAD的影响及其机制。方法：检测HSP90AB1、HNRNPH1、自噬相关蛋白MAP1LC3B在LUAD中的表达及作用。此外，我们还利用生物信息学分析、沉默和过表达技术以及体内模型来探索这些蛋白在LUAD进展中的调控机制。结果：HSP90AB1在LUAD中高表达，与较差的预后相关。过表达HSP90AB1可显著促进LUAD细胞的恶性表型，抑制map1lc3b介导的自噬。而HNRNPH1过表达可逆转HSP90AB1过表达导致的恶性表型，通过结合HSP90AB1 mRNA并抑制其蛋白表达，促进map1lc3b介导的自噬。动物实验也显示过表达HNRNPH1可通过促进细胞自噬抑制肿瘤进展。结论：我们验证了HSP90AB1、HNRNPH1和MAP1LC3B在LUAD中的关键作用，并揭示了可能的调控机制，即HNRNPH1通过HSP90AB1/MAP1LC3B轴促进自噬来抑制LUAD的发展。这些发现可能为改善LUAD的治疗和预后提供新的见解。临床试验号：不适用。

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

Respiratory Research RESPIRATORY SYSTEM-

CiteScore

9.70

自引率

1.70%

发文量

314

审稿时长

4-8 weeks

期刊介绍： Respiratory Research publishes high-quality clinical and basic research, review and commentary articles on all aspects of respiratory medicine and related diseases. As the leading fully open access journal in the field, Respiratory Research provides an essential resource for pulmonologists, allergists, immunologists and other physicians, researchers, healthcare workers and medical students with worldwide dissemination of articles resulting in high visibility and generating international discussion. Topics of specific interest include asthma, chronic obstructive pulmonary disease, cystic fibrosis, genetics, infectious diseases, interstitial lung diseases, lung development, lung tumors, occupational and environmental factors, pulmonary circulation, pulmonary pharmacology and therapeutics, respiratory immunology, respiratory physiology, and sleep-related respiratory problems.