Upregulation of LPGAT1 Enhances Lung Adenocarcinoma Proliferation

LPGAT1 上调促进肺腺癌增殖

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作者:Huiyuan Gong, Chao Ma, Xiaojun Li, Xueying Zhang, Linxiang Zhang, Pengfei Chen, Wei Wang, Yannan Hu, Ting Huang, Nan Wu, Xiaojing Wang

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.

Conclusions

This study demonstrates that LPGAT1 promotes proliferation and inhibits apoptosis in LUAD. Hence, LPGAT1 may provide new treatment strategies for LUAD.

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.

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