Research Paper Volume 15, Issue 21 pp 12451—12475
Abnormal low expression of SFTPC promotes the proliferation of lung adenocarcinoma by enhancing PI3K/AKT/mTOR signaling transduction
- 1 Henan Key Laboratory of Immunology and Targeted Drugs, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan, China
- 2 Department of Geriatrics, Xijing Hospital, The Air Force Military Medical University, Xi’an, Shaanxi, China
- 3 Department of Blood Transfusion, Shanxi Provincial People’s Hospital, Affiliate of Shanxi Medical University, Taiyuan, Shanxi, China
- 4 Department of Geriatric Medicine, Shanxi Provincial People’s Hospital, Affiliate of Shanxi Medical University, Taiyuan, Shanxi, China
- 5 Department of Ultrasound, Shanxi Provincial People’s Hospital, Affiliate of Shanxi Medical University, Taiyuan, Shanxi, China
- 6 Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi’an, Shaanxi, China
- 7 Department of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China
- 8 College of Management, Zhejiang Shuren University, Hangzhou, Zhejiang, China
- 9 College of Life Science and Agronomy, Zhoukou Normal University, Zhoukou, Henan, China
- 10 MOE Key Laboratory of Modern Teaching Technology, Center for Teacher Professional Ability Development, Shaanxi Normal University, Xi’an, Shaanxi, China
- 11 Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan, China
Received: June 23, 2023 Accepted: October 3, 2023 Published: November 12, 2023
https://doi.org/10.18632/aging.205191How to Cite
Copyright: © 2023 Zuo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The abnormality of surfactant protein C (SFTPC) has been linked to the development of a number of interstitial lung diseases, according to mounting evidence. Nonetheless, the function and mechanism of SFTPC in the biological progression of lung adenocarcinoma (LUAD) remain unclear. Analysis of public datasets and testing of clinical samples suggested that SFTPC expression was abnormally low in LUAD, which was associated with the onset and poor prognosis of LUAD. The SFTPC-related risk score was derived using least absolute shrinkage and selection operator Cox regression as well as multivariate Cox regression. The risk score was highly correlated with tumor purity and tumor mutation burden, and it could serve as an independent prognostic indicator for LUAD. Low-risk LUAD patients may benefit more from CTLA-4 or/and PD-1 inhibitors. Overall, the risk score is useful for LUAD patient prognostication and treatment guidance. Moreover, in vitro and in vivo experiments demonstrated that SFTPC inhibits the proliferation of LUAD by inhibiting PI3K/AKT/mTOR signaling transduction. These results reveal the molecular mechanism by which SFTPC inhibits the proliferation of LUAD and suggest that SFTPC could be a new therapeutic target for LUAD.