TMEM176B Promotes EMT via FGFR/JNK Signalling in Development and Tumourigenesis of Lung Adenocarcinoma

Author:

Sun Ping-Hui123ORCID,Xia Siyu4,Yuan Runzhu5,Zhang Bin1ORCID,Wang Guangsuo1

Affiliation:

1. Department of Thoracic Surgery, The Second Clinical Medical College of Jinan University, Shenzhen People’s Hospital, Shenzhen 518000, China

2. Integrated Chinese and Western Medicine Postdoctoral Research Station, Jinan University, Guangzhou 510632, China

3. Division of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK

4. Department of Reproductive Medicine, Dongguan Maternal and Child Health Care Hospital, Dongguan 523000, China

5. School of Medicine, The First Affiliated Hospital of Southern University of Science and Technology, Shenzhen People’s Hospital, Shenzhen 518000, China

Abstract

Lung cancer, the leading cause of cancer-related incidence and mortality worldwide, is characterised by high invasiveness and poor prognosis. Novel therapeutic targets are required, especially for patients with inoperable metastatic disease requiring systemic therapies to improve patients’ welfare. Recently, studies indicated that TMEM176B is a positive regulator in breast and gastric cancers, and it could be a potential target for treatment. In this study, we used single-cell sequencing, proteomics, Co-IP, and in vivo and in vitro experimental models to investigate the role of TMEM176B in lung adenocarcinoma development. Our study indicated that TMEM176B expression was enhanced in lung adenocarcinoma tissues, and it was associated with shorter overall survival (OS). TMEM176B promoted cellular functions, including cell proliferation, invasion, migration and adhesion in vitro and tumour growth in vivo. Moreover, the tube formation ability of endothelial cells was enhanced by treating with the tumour cell-conditioned medium. We have also demonstrated that TMEM176B regulated EMT via the FGFR1/JNK/Vimentin/Snail signalling cascade. Overall, our study suggests TMEM176B could be a potential therapeutic target in lung adenocarcinoma.

Funder

Shenzhen Science and Technology Innovation Committee

National Natural Science Foundation of China

Guangdong Basic and Applied Basic Research Foundation

Shenzhen-Hong Kong-Macau Science and Technology Programme

Shenzhen People’s Hospital Clinical Scientist Programme

Publisher

MDPI AG

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