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BKS-112, a Selective Histone Deacetylase 6 Inhibitor, Suppresses Triple-Negative Breast Cancer Cells via AKT/mTOR

Sreevarsha Gali1,2, Swati Sharma1, Hyunji Noh1

  • 1School of Pharmacy, Sungkyunkwan University, 2066, Seobu-ro, Jangan-gu, Suwon 16419, Republic of Korea.

Antioxidants (Basel, Switzerland)
|November 27, 2025
PubMed

Insights

The novel histone deacetylase 6 (HDAC6) inhibitor, BKS-112, shows significant anticancer effects against triple-negative breast cancer (TNBC). It effectively reduces cell viability, induces apoptosis and autophagy, and inhibits metastasis, offering therapeutic promise for TNBC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Triple-negative breast cancer (TNBC) presents a significant clinical challenge due to its aggressive nature and lack of targeted therapies.
  • The absence of estrogen receptor (ER), progesterone receptor (PR), and HER2 expression in TNBC limits treatment options, leading to poorer patient outcomes.
  • Histone deacetylase 6 (HDAC6) is implicated in cancer progression and represents a potential therapeutic target.

Purpose of the Study:

  • To investigate the anticancer potential of BKS-112, a novel HDAC6 inhibitor, against triple-negative breast cancer (TNBC) cells.
  • To elucidate the molecular mechanisms underlying BKS-112's effects on TNBC cell viability, apoptosis, autophagy, cell cycle, and migration.
  • To assess the prognostic significance of HDAC protein expression in TNBC.

Main Methods:

  • In vitro studies using MDA-MB-231 TNBC cell line.
  • Assessment of cell viability, apoptosis, autophagy, cell cycle progression, and colony formation assays.
  • Analysis of protein expression, acetylation levels, enzyme activity, and signaling pathway modulation (e.g., PI3K/AKT).

Main Results:

  • BKS-112 demonstrated dose- and time-dependent inhibition of TNBC cell viability and colony formation.
  • The compound induced significant morphological changes, G1 cell cycle arrest, and apoptosis via mitochondrial pathways.
  • BKS-112 increased histone and α-tubulin acetylation, downregulated HDAC6 activity, reduced cell migration, and triggered autophagy.
  • Elevated reactive oxygen species (ROS) and modulation of PI3K/AKT signaling were observed.

Conclusions:

  • BKS-112 exhibits potent anticancer activity against TNBC by inducing cell cycle arrest, apoptosis, and autophagy.
  • The inhibition of HDAC6 and subsequent molecular changes contribute to BKS-112's anti-TNBC effects.
  • BKS-112 represents a promising therapeutic candidate for the treatment of triple-negative breast cancer.
Keywords:
BKS-112HDAC6TNBCapoptosisautophagyreactive oxygen species

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