LncRNA GAS5 attenuates COPD pathogenesis by stabilizing p120 catenin to suppress NF-κB-driven inflammation

Sep 30, 2026

Uploaded by jayni

Objective to determine the role of lncRNA GAS5 in COPD and define the underlying mechanism. Methods use a COPD mouse model and in vitro inflammatory models created by CSE stimulation in 16HBE and BEAS-2B cells. GAS5 or GAS5 shRNA is delivered via recombinant adenoviruses to overexpress or knock down GAS5. RT-PCR and Western blot measure p120/NF-κB, while NF-κB p65 distribution is assessed by blot and immunofluorescence. IL-6, IL-8, and TNF-α are quantified by RT-PCR and ELISA. Results show GAS5 downregulation in COPD and that GAS5 overexpression alleviates inflammation by regulating NF-κB through binding p120.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages12

Reading Time30 min

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Introduction

COPD and airway inflammation background

Airway epithelial barrier and p120 catenin

NF-κB signaling and inflammatory amplification

Abstract

Objective

Methods

Results

Conclusion

Zhang et al. Respiratory Research (2026) 27:9 [https://doi.org/10.1186/s12931-025-03445-w](https://doi.org/10.1186/s12931-025-03445-w) Respiratory Research RESEARCH Open Access LncRNA GAS5 attenuates COPD pathogenesis by stabilizing p120 catenin to suppress NF-κBdriven inflammation Chao Zhang 1*†, Xiaoqian Zhan 1†, Yue Li2, Zhe Zheng2, Xiaoyang Ji2*, Liuye Yang3* and Xi Wang 1* Abstract Objective To investigate the role of lncRNA GAS5 in COPD and its underlying mechanism. Methods COPD mouse model was conducted as an in vivo inflammatory response model. CSE was used to stimulate human airway epithelial cells (16HBE) and human normal lung epithelial cells (BEAS-2B) to establish an in vitro inflammatory response model. Recombinant adenoviruses containing GAS5 or GAS5 shRNA were used to overexpression or knockdown of GAS5 . The expression of p120/NF-κB was detected by RT-PCR and Western Blot. The distribution of NF-κB p65 protein in cells was detected by western blot and immunofluorescence staining. The expression levels of IL-6, IL-8 and TNF-α in downstream NF-κB were detected by RT-PCR and ELISA. Result The expression of lncRNA GAS5 was downregulated in COPD in vivo and in vitro. We showed that overexpression of GAS5 alleviates inflammation and NF-κB activation in COPD in vivo and in vitro. Moreover, we demonstrated that GAS5 regulate NF-κB activation by bind with p120 . Knocking down of p120 inhibits the protective effect of GAS5 on inflammation. Conclusion LncRNA GAS5 can bind with p120, enhance p120 stability and inhibit the NF-κB pathway and production of inflammatory factors downstream of NF-κB, thus playing a protective role in the airway. Keywords COPD, LncRNA GAS5, P120 catenin, NF-κB, Inflammation †Chao Zhang and Xiaoqian Zhan contributed equally as the first authors. *Correspondence: Chao Zhang [zhangchao1@hust.edu.cn](zhangchao1@hust.edu.cn)[ ](zhangchao1@hust.edu.cn)Xiaoyang Ji [xy15836170012@163.com](xy15836170012@163.com)[ ](xy15836170012@163.com)Liuye Yang [2025xh8051@hust.edu.cn](2025xh8051@hust.edu.cn) Xi Wang [xwang@tjmu.edu.cn](xwang@tjmu.edu.cn) 1Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Ave, Wuhan 430030, China 2Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, No. 1, Jianshe East Road, Zhengzhou 450052, China 3Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Ave, Wuhan 430022, China © The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creati](http://creati)[vecommons.org/l](vecommons.org/l)icenses/by-nc-nd/4.0/. Zhang et al. Respiratory Research (2026) 27:9 Introduction Chronic obstructive pulmonary disease (COPD), is a group of chronic airway obstructive diseases. It progresses slowly and is characterized by irreversible airflow restriction, which will eventually lead to chronic respiratory failure [1]. Currently

FAQs

What is the primary objective of the study on lncRNA GAS5 in COPD?

To investigate the role of lncRNA GAS5 in COPD and clarify its underlying mechanism.

How were inflammation models established for in vitro experiments?

CSE was used to stimulate human airway epithelial cells (16HBE) and human normal lung epithelial cells (BEAS-2B) to establish an in vitro inflammatory response model.

What mechanism does the study propose for how GAS5 suppresses inflammation?

GAS5 binds with p120, enhances p120 stability, and inhibits the NF-κB pathway, thereby reducing downstream inflammatory factor production. Knocking down p120 blocks GAS5’s protective effect.

Sep 30, 2026

Uploaded by jayni