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Mocetinostat (MGCD0103) induced autophagy in SKBR-3 breast cancer cells by regulating ROS/MAPK pathway

Hacer Kaya Çakir1,2, Onur Eroglu1,2

  • 1Department of Molecular Biology and Genetics, Faculty of Science, Bilecik Seyh Edebali University, Turkey.

Journal of Investigative Medicine : the Official Publication of the American Federation for Clinical Research
|February 25, 2026
PubMed

Insights

Mocetinostat, a histone deacetylase inhibitor, suppresses breast cancer cell growth by inducing ROS-mediated autophagy via the MAPK pathway. This research clarifies its anticancer mechanisms, offering potential new therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer is a leading global cause of cancer mortality.
  • Mocetinostat (MGCD0103) is a histone deacetylase inhibitor with known antitumor effects, but its role in breast cancer requires further elucidation.
  • Understanding the interplay between reactive oxygen species (ROS), mitogen-activated protein kinase (MAPK) signaling, and autophagy is crucial for breast cancer treatment.

Purpose of the Study:

  • To investigate the mechanisms of action of mocetinostat in breast cancer cells.
  • To clarify the relationship between ROS/MAPK signaling, autophagy, and autophagic cell death induced by mocetinostat.
  • To evaluate mocetinostat's therapeutic potential in breast cancer.

Main Methods:

  • MTT and wound healing assays were used to assess cell viability and proliferation.
  • ROS and autophagy levels were quantified using assay kits.
  • Western blotting was employed to evaluate MAPK signaling pathway activation and protein expression.

Main Results:

  • Mocetinostat demonstrated dose- and time-dependent inhibition of breast cancer cell viability and migration.
  • Treatment with mocetinostat led to increased ROS accumulation and induced autophagy in SKBR-3 cells.
  • Mocetinostat modulated key signaling proteins, including downregulation of PI3K, AKT, ERK1/2, SAPK/JNK, and c-Jun, and upregulation of P53 and ATG5.

Conclusions:

  • Mocetinostat suppresses breast cancer cell proliferation and migration in vitro.
  • The anticancer effects of mocetinostat are mediated through a ROS-dependent autophagy mechanism involving the MAPK pathway.
  • These findings highlight mocetinostat's potential as a novel therapeutic agent for breast cancer.
Keywords:
HDACiROS/MAPK pathwayautophagybreast cancermocetinostat

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