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Curcumin enhances the anticancer effects of trichostatin a in breast cancer cells

Guang Yan1, Kimmer Graham, Susan Lanza-Jacoby

  • 1Department of Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

Molecular Carcinogenesis
|February 1, 2012
PubMed

Insights

Combining Tricostatin A (TSA) and curcumin shows promise for breast cancer treatment. This combination effectively reduced cancer cell growth and induced apoptosis, offering a potential new therapeutic strategy for aggressive breast cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • HER-2 positive and estrogen receptor-negative breast cancers exhibit aggressive behavior and poor response to standard treatments.
  • Histone deacetylase (HDAC) inhibitors and curcumin demonstrate potential anticancer properties, including reduced cell survival and induction of apoptosis.
  • Investigating combination therapies is crucial for improving outcomes in challenging breast cancer subtypes.

Purpose of the Study:

  • To evaluate the synergistic antiproliferative and apoptotic effects of combining the HDAC inhibitor Tricostatin A (TSA) with curcumin in breast cancer cells.
  • To elucidate the molecular mechanisms underlying the combined effects of TSA and curcumin on cell viability, cell cycle, and apoptosis.

Main Methods:

  • Treatment of SkBr3 and 435eB breast cancer cells with varying concentrations of TSA and curcumin.
  • Assessment of cell viability, proliferation, and apoptosis using biochemical assays.
  • Analysis of key protein expression involved in cell cycle regulation (p21, p27, Cyclin D1), apoptosis (caspase 3, PARP-1, Bcl2 family proteins), and signaling pathways (ERK, Akt, JNK, p38).
  • Pharmacological inhibition of JNK and p38 pathways to determine their role in the observed effects.

Main Results:

  • The combination of TSA and curcumin significantly enhanced antiproliferative and apoptotic effects compared to individual agents, particularly at higher curcumin concentrations (10-20 µM).
  • Combination treatment led to decreased phosphorylation of ERK and Akt, G0/G1 cell cycle arrest, and altered expression of cell cycle regulators (increased p21/p27, decreased Cyclin D1).
  • Apoptosis was confirmed by caspase 3 and PARP-1 cleavage, with no significant changes in Bcl2 family proteins and decreased p53. JNK pathway activation was crucial, as JNK inhibition attenuated the decreased viability.

Conclusions:

  • The combination of curcumin and TSA induces p53-independent apoptosis in breast cancer cells, primarily through JNK pathway activation.
  • These findings support the potential of combining curcumin with TSA as a therapeutic strategy for aggressive breast cancers.
  • Further exploration of this combination therapy is warranted for clinical application in breast cancer treatment.

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