LPCAT1 overexpression promotes the progression of hepatocellular carcinoma

被引:34
|
作者
He, Rong-Quan [1 ]
Li, Jian-Di [2 ]
Du, Xiu-Fang [2 ]
Dang, Yi-Wu [2 ]
Yang, Lin-Jie [2 ]
Huang, Zhi-Guang [2 ]
Liu, Li-Min [3 ]
Liao, Liu-Feng [4 ]
Yang, Hong [5 ]
Chen, Gang [2 ]
机构
[1] Guangxi Med Univ, Dept Oncol, Affiliated Hosp 1, 6 Shuangyong Rd, Nanning 530021, Guangxi Zhuang, Peoples R China
[2] Guangxi Med Univ, Dept Pathol, Affiliated Hosp 1, 6 Shuangyong Rd, Nanning 530021, Guangxi Zhuang, Peoples R China
[3] Guangxi Med Univ, Coll Pharm, Dept Toxicol, 22 Shuangyong Rd, Nanning 530021, Guangxi Zhuang, Peoples R China
[4] Guangxi Med Univ, Dept Pharm, Canc Hosp, 71 Hedi Rd, Nanning 530021, Guangxi Zhuang, Peoples R China
[5] Guangxi Med Univ, Ultrason Div, Affiliated Hosp 1, Radiol Dept, 6 Shuangyong Rd, Nanning 530021, Guangxi Zhuang, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Hepatocellular carcinoma; Lysophosphatidylcholine acyltransferase 1; Functional experiment; Molecular mechanism; Clinical applications; HISTONE DEACETYLASE INHIBITORS; CELL-CYCLE; PROLIFERATION; CONTRIBUTES; APOPTOSIS;
D O I
10.1186/s12935-021-02130-4
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
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页数:17
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