4.7 Article

LPCAT1 overexpression promotes the progression of hepatocellular carcinoma

期刊

CANCER CELL INTERNATIONAL
卷 21, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12935-021-02130-4

关键词

Hepatocellular carcinoma; Lysophosphatidylcholine acyltransferase 1; Functional experiment; Molecular mechanism; Clinical applications

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资金

  1. Fund of National Natural Science Foundation of China [NSFC82160762]
  2. Natural Science Foundation of Guangxi, China [2018GXNSFAA294025]
  3. Guangxi Medical High-level Key Talents Training 139 Program
  4. Guangxi Medical University Training Program for Distinguished Young Scholars
  5. Medical Excellence Award - Creative Research Development Grant from the First Affiliated Hospital of Guangxi Medical University
  6. Guangxi Educational Science Planning Key Project [2021B167]
  7. Guangxi Higher Education Undergraduate Teaching Reform Project [2020JGA146]
  8. Guangxi Medical University Education and Teaching Reform Project [2019XJGZ04]
  9. China Postdoctoral Science Foundation [2021M693804]
  10. Guangxi Zhuang Autonomous Region Health Committee Self-financed Scientific Research Project [Z20201147]
  11. Guangxi Medical University Student Innovation and Entrepreneurship Training Program Project [202010598002]

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This study revealed that increased LPCAT1 expression correlated with poor prognosis in HCC patients and promoted HCC progression by enhancing cellular growth, migration, and metastasis. The cell cycle and chemical carcinogenesis were identified as the most enriched signaling pathways.
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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