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Terminalia catappa attenuates urokinase-type plasminogen activator expression through Erk pathways in Hepatocellular

Chao-Bin Yeh, Yung-Luen Yu, Chiao-Wen Lin

  • 1Cancer Research Center, Changhua Christian Hospital, Changhua, Taiwan. 170780@cch.org.tw.

BMC Complementary and Alternative Medicine
|June 3, 2014
PubMed
Abstract

Insights

Terminalia catappa leaf extract (TCE) inhibits hepatocellular carcinoma (HCC) metastasis by reducing urokinase-type plasminogen activator (u-PA) expression and activity. This study elucidates the molecular mechanisms behind TCE

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hepatocellular carcinoma (HCC) metastasis significantly impacts patient survival rates.
  • Terminalia catappa leaf extract (TCE) has demonstrated antimetastasis effects on HCC cells.
  • The precise molecular mechanisms of urokinase-type plasminogen activator (u-PA) in HCC metastasis require further investigation.

Purpose of the Study:

  • To investigate the molecular mechanisms by which TCE suppresses HCC metastasis.
  • To determine the role of urokinase-type plasminogen activator (u-PA) in TCE-mediated antimetastasis effects.
  • To explore the impact of TCE on u-PA expression and its regulatory pathways in HCC.

Main Methods:

  • Casein zymography and western blotting were used to assess u-PA activity and protein levels.
  • Real-time PCR and promoter assays were employed to detect transcriptional levels of u-PA.
  • Chromatin immunoprecipitation (ChIP) assays were performed to analyze the binding of transcription factors to the u-PA promoter.
  • Western blotting was used to evaluate the phosphorylation status of the ERK1/2 pathway.

Main Results:

  • TCE treatment significantly reduced u-PA activity, protein levels, and mRNA levels in Huh7 HCC cells.
  • TCE inhibited the transcriptional activity of nuclear factors SP-1 and NF-κB, which are involved in u-PA gene regulation.
  • TCE suppressed u-PA effects by reducing the phosphorylation of the ERK1/2 signaling pathway.

Conclusions:

  • u-PA expression is a critical target for TCE-mediated suppression of HCC metastasis.
  • TCE exerts its antimetastasis effects through the downregulation of u-PA via SP-1, NF-κB, and ERK1/2 pathways.
  • Targeting u-PA represents a promising therapeutic strategy for managing HCC metastasis with TCE.

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