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Helichrysetin Induces DNA Damage that Triggers JNK-Mediated Apoptosis in Ca Ski Cells

Ho Yen Fong1, Sri Nurestri Abd Malek1, Hui Shin Yee1

  • 1Institute of Biological Sciences, Faculty of Science, University of Malaya, 50603 Kuala Lumpur, Malaysia.

Pharmacognosy Magazine
|December 5, 2017
PubMed
Abstract

Insights

Helichrysetin, a natural chalcone, effectively inhibits cervical cancer cells by inducing DNA damage and apoptosis through a JNK-mediated pathway. This discovery highlights its potential as a novel anticancer therapeutic agent for cervical cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Cervical cancer is a leading cause of cancer in women with limited treatment options.
  • Naturally occurring chalcones, like helichrysetin, show promise as anticancer agents.
  • Helichrysetin exhibits potent antiproliferative activity against human cancer cells.

Purpose of the Study:

  • To investigate the anticancer effects of helichrysetin on cervical cancer cells.
  • To elucidate the mechanism of helichrysetin-induced apoptosis.
  • To assess the role of the c-Jun N-terminal kinase (JNK) pathway in helichrysetin's action.

Main Methods:

  • Evaluation of helichrysetin's inhibitory activity at various concentrations.
  • Assessment of apoptosis induction using flow cytometry.
  • Western blotting to analyze JNK-mediated apoptosis and related protein expression.

Main Results:

  • Helichrysetin inhibited Ca Ski cervical cancer cells with a half maximal inhibitory concentration (IC50) of 30.62 ± 0.38 μM.
  • The compound induced DNA damage, mitochondrial membrane disruption, and loss of cell membrane integrity.
  • Apoptosis was mediated by JNK activation, leading to increased Bax and caspase 3, and decreased Bcl-2 expression, alongside ATM phosphorylation.

Conclusions:

  • Helichrysetin inhibits Ca Ski cells via a DNA damage-induced, JNK-mediated apoptotic pathway.
  • This mechanism involves the activation of the p53-downstream apoptotic pathway.
  • Helichrysetin demonstrates potential as an anticancer agent for cervical cancer by inducing JNK-activated apoptosis.
Keywords:
ApoptosisCa Skic-Jun N-terminal kinase pathwayhelichrysetin

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