IMR Press / FBL / Volume 28 / Issue 5 / DOI: 10.31083/j.fbl2805089
Open Access Original Research
Upregulation of LPGAT1 Enhances Lung Adenocarcinoma Proliferation
Show Less
1 Department of Thoracic Surgery, First Affiliated Hospital, Bengbu Medical College, 233000 Bengbu, Anhui, China
2 Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease Bengbu Medical College, 233000 Bengbu, Anhui, China
3 Molecular Diagnosis Center, First Affiliated Hospital, Bengbu Medical College, 233000 Bengbu, Anhui, China
4 Department of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Bengbu Medical College, 233000 Bengbu, Anhui, China
*Correspondence: bbmcwunan@163.com (Nan Wu); wangxiaojing8888@163.com (Xiaojing Wang)
These authors contributed equally.
Front. Biosci. (Landmark Ed) 2023, 28(5), 89; https://doi.org/10.31083/j.fbl2805089
Submitted: 15 November 2022 | Revised: 3 March 2023 | Accepted: 14 March 2023 | Published: 11 May 2023
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.
Abstract

Background: Lung adenocarcinoma (LUAD) is one of the leading causes of cancer-related mortality. Lysophosphatidylglycerol acyltransferase (LPGAT1) regulates the biosynthesis of triacylglycerol, which is essential for maintaining phospholipid homeostasis and modulating the structural integrity of mitochondrial membranes. LPGAT1 has been demonstrated to be differentially expressed in normal lung tissue and LUAD tissues, and can serve as a metabolically relevant gene with potential prognostic value. However, the potential role of LPGAT1 in LUAD is still unknown. This study sought to determine the role of LPGAT1 in LUAD progression. Methods: LPGAT1 expression was examined in LUAD cells and tumor tissues from LUAD patients. The effect of LPGAT1 was then assessed in both cell and animal models after LPGAT1 was knocked down by RNA interference. Results: LPGAT1 was upregulated in LUAD tissues. Overexpression of LPGAT1 was associated with an unfavorable prognosis in LUAD patients, as revealed by univariate and multivariate Cox analyses. Knockdown of LPGAT1 abrogated tumor growth and proliferation in both cell and animal models. Conclusions: This study demonstrates that LPGAT1 promotes proliferation and inhibits apoptosis in LUAD. Hence, LPGAT1 may provide new treatment strategies for LUAD.

Keywords
lung adenocarcinoma
LPGAT1
phosphatidylglycerol metabolic process
lung cancer
Funding
KJ2020A0575/Key Program of Natural Science Research of Higher Education of Anhui Province
82072585/National Natural Science Foundation of China
202003a07020024/Anhui Provincial Major Science and Technology Project
Figures
Fig. 1.
Share
Back to top