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Emodin-induced apoptosis through p53-dependent pathway in human hepatoma cells

Den-En Shieh1, Yuan-Ying Chen, Ming-Hong Yen

  • 1Graduate Institute of Pharmaceutical Sciences, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC.

Life Sciences
|February 28, 2004
PubMed

Insights

Emodin effectively inhibits human hepatoma cell growth by inducing apoptosis and cell cycle arrest. This natural compound activates key signaling pathways, suggesting its potential as a hepatocellular carcinoma (HCC) therapeutic agent.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Cytotoxic anticancer drugs often induce apoptosis, but their signaling pathways are not fully understood.
  • Hepatocellular carcinoma (HCC) remains a significant health concern, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To investigate the cytotoxic effects of emodin on human hepatoma cell lines.
  • To elucidate the underlying molecular mechanisms of emodin-induced apoptosis and cell cycle arrest.

Main Methods:

  • Assessing emodin's cytotoxic effect using IC(50) values on HepG2/C3A, PLC/PRF/5, and SK-HEP-1 cells.
  • Analyzing DNA fragmentation and sub-G(1) cell cycle accumulation to confirm apoptosis.
  • Evaluating cell cycle progression and expression of apoptosis-related proteins (p53, p21, Fas, caspase-3).

Main Results:

  • Emodin demonstrated significant inhibitory effects on hepatoma cell lines with determined IC(50) values.
  • Apoptosis was confirmed in HepG2/C3A cells via DNA fragmentation and sub-G(1) phase accumulation.
  • Emodin treatment led to G(2)/M phase cell cycle arrest and increased levels of p53, p21, Fas, and caspase-3.

Conclusions:

  • Emodin effectively inhibits human hepatoma cell growth and induces apoptosis.
  • The mechanism involves p53 and p21 activation, leading to G(2)/M cell cycle arrest.
  • Emodin shows promise as a chemotherapeutic agent for hepatocellular carcinoma (HCC).

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