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Parthenolide-induced apoptosis, autophagy and suppression of proliferation in HepG2 cells. | LitMetric

Parthenolide-induced apoptosis, autophagy and suppression of proliferation in HepG2 cells.

Asian Pac J Cancer Prev

National Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun, China E-mail :

Published: March 2015

AI Article Synopsis

  • * Researchers used various methods to assess cell viability, apoptosis, and autophagy, finding that parthenolide effectively inhibited growth and increased apoptosis markers in HepG2 cells.
  • * The findings suggest that parthenolide combats cancer by triggering cell death, promoting autophagy, and reducing the expression of growth-related genes.

Article Abstract

Purpose: To investigate the anticancer effects and underlying mechanisms of parthenolide on HepG2 human hepatocellular carcinoma cells.

Materials And Methods: Cell viability was assessed by MTT assay and cell apoptosis through DAPI, TUNEL staining and Western blotting. Monodansylcadaverin(MDC) and AO staining were used to detect cell autophagy. Cell proliferation was assessed by Ki67 immunofluorescence staining.

Results: Parthenolide induced growth inhibition in HepG2 cells. DAPI and TUNEL staining showed that parthenolide could increase the number of apoptotic nuclei, while reducing the expression of the anti-apoptotic protein Bcl-2 and elevating the expression of related proteins, like p53, Bax, cleaved caspase9 and cleaved caspase3. Parthenolide could induce autophagy in HepG2 cells and inhibited the expression of proliferation-related gene, Ki-67.

Conclusions: Parthenolide can exert anti-cancer effects by inducing cell apoptosis, activating autophagy and inhibiting cell proliferation.

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Source
http://dx.doi.org/10.7314/apjcp.2014.15.12.4897DOI Listing

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