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Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis

  • 0Department of Pathology and Hepatology, The Fifth Medical Center of Chinese PLA General Hospital, Beijing 100039, China.
World Journal of Gastrointestinal Oncology +

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August 22, 2024

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August 22, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Lecithin-cholesterol acyltransferase (LCAT) is downregulated in hepatocellular carcinoma (HCC), inhibiting metastasis by suppressing PI3K/AKT/mTOR signaling. LCAT serves as a prognostic marker and potential therapeutic target for HCC.

Area Of Science

  • Oncology
  • Molecular Biology
  • Biochemistry

Background

  • Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality globally.
  • Metastasis in HCC is a primary driver of early recurrence and poor patient outcomes.
  • The molecular mechanisms underlying HCC metastasis remain incompletely understood.

Purpose Of The Study

  • To elucidate the role of lecithin-cholesterol acyltransferase (LCAT) in HCC metastasis.
  • To identify potential therapeutic targets for mitigating HCC progression.
  • To establish a theoretical framework for novel HCC treatment strategies.

Main Methods

  • LCAT was identified as a candidate gene through gene microarray and bioinformatics analysis.
  • LCAT expression was quantified in clinical HCC samples using qPCR and Western blotting.
  • In vitro and in vivo assays assessed LCAT's impact on HCC cell proliferation, migration, invasion, and tumor formation, including PI3K/AKT/mTOR pathway analysis.
  • Machine learning models were developed to predict HCC metastasis risk.

Main Results

  • LCAT was significantly downregulated in HCC tissues, correlating with increased recurrence, metastasis, and poorer prognosis.
  • LCAT suppressed HCC cell proliferation, migration, and invasion in vitro and in vivo.
  • LCAT expression negatively correlated with HCC tumor size and metastatic status.
  • A predictive model incorporating LCAT, TNM stage, and alpha-fetoprotein levels demonstrated efficacy in identifying high-risk HCC patients for metastasis.

Conclusions

  • LCAT is downregulated in HCC at both translational and protein levels, suggesting a role in inhibiting tumor metastasis.
  • LCAT may exert its anti-metastatic effects by attenuating the PI3K/AKT/mTOR signaling pathway.
  • LCAT represents a promising prognostic biomarker and a potential therapeutic target for hepatocellular carcinoma.

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