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LPCAT1 overexpression promotes the progression of hepatocellular carcinoma

Authors :
Rong-Quan He
Jian-Di Li
Xiu-Fang Du
Yi-Wu Dang
Lin-Jie Yang
Zhi-Guang Huang
Li-Min Liu
Liu-Feng Liao
Hong Yang
Gang Chen
Source :
Cancer Cell International, Vol 21, Iss 1, Pp 1-17 (2021)
Publication Year :
2021
Publisher :
BMC, 2021.

Abstract

Abstract Background Hepatocellular carcinoma (HCC) remains one of the most common malignant neoplasms. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) plays a key role in the lipid remodelling and is correlated with various neoplasms. Nonetheless, the biological functions and molecular mechanisms of LPCAT1 underlying HCC remain obscure. Methods In the present study, we investigated the role of LPCAT1 in the progression of HCC. In-house RT-qPCR, tissue microarrays, and immunohistochemistry were performed to detect the expression levels and the clinical value of LPCAT1 in HCC. External datasets were downloaded to confirm the results. Proliferation, migration, invasiveness, cell cycle, and apoptosis assays were conducted to reveal the biological effects LPCAT1 has on SMMC-7721 and Huh7 cells. HCC differentially expressed genes and LPCAT1 co-expressed genes were identified to explore the molecular mechanisms underlying HCC progression. Results LPCAT1 showed upregulated expression in 3715 HCC specimens as opposed to 3105 non-tumour specimens. Additionally, LPCAT1 might be an independent prognostic factor for HCC. LPCAT1-knockout hampered cellular proliferation, migration, and metastasis in SMMC-7721 and Huh7 cells. More importantly, the cell cycle and chemical carcinogenesis were the two most enriched signalling pathways. Conclusions The present study demonstrated that increased LPCAT1 correlated with poor prognosis in HCC patients and fuelled HCC progression by promoting cellular growth, migration, and metastasis.

Details

Language :
English
ISSN :
14752867
Volume :
21
Issue :
1
Database :
Directory of Open Access Journals
Journal :
Cancer Cell International
Publication Type :
Academic Journal
Accession number :
edsdoj.0fe3d6f393394ab3a2d3ae5b3b19b196
Document Type :
article
Full Text :
https://doi.org/10.1186/s12935-021-02130-4