Curcumin induces apoptosis through mitochondrial pathway and caspases activation in human melanoma cells

Mol Biol Rep. 2015 Jan;42(1):267-75. doi: 10.1007/s11033-014-3769-2. Epub 2014 Sep 28.


Melanoma is the most malignant skin cancer and is highly resistant to chemotherapy and radiotherapy. Curcumin is a component of turmeric, the yellow spice derived from the rhizome of Curcuma longa. It has been demonstrated to modulate multiple cell signaling pathways, including apoptosis, proliferation, angiogenesis and inflammation. In this study, we studied the signaling pathways involved in melanoma cell death after treatment with curcumin using western blotting. Colorimetric assays (MTT) assessed cell viability. Flow cytometry and DNA laddering evaluated cell apoptosis. Fluorescent microscopy was used to evaluate of Hoechst 33342 staining of nuclei. The result demonstrated that curcumin could induce apoptosis and inhibit proliferation in melanoma cells. Curcumin stimulated the expression of pro-apoptotic Bax, and inhibited the activation of anti-apoptotic Mcl-1 and Bcl-2. During curcumin treatment, caspase-8 and Caspase-3 were cleaved in time and dose-dependent manners. Curcumin treatment also altered the expressions of apoptosis associated proteins NF-κB, p38 and p53. Curcumin induced DNA double strand breaks, which were indicated by phosphorylated H2AX. Our data suggested that curcumin could be used as a novel and effective approach for the treatment of melanoma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Annexin A5 / metabolism
  • Apoptosis / drug effects*
  • Caspases / metabolism*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Curcumin / chemistry
  • Curcumin / pharmacology*
  • DNA Breaks, Double-Stranded / drug effects
  • DNA Fragmentation / drug effects
  • Dose-Response Relationship, Drug
  • Enzyme Activation / drug effects
  • Flow Cytometry
  • Humans
  • Melanoma / enzymology*
  • Melanoma / pathology*
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • NF-kappa B / metabolism
  • Propidium / metabolism
  • Time Factors
  • Tumor Suppressor Protein p53 / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Annexin A5
  • NF-kappa B
  • Tumor Suppressor Protein p53
  • Propidium
  • p38 Mitogen-Activated Protein Kinases
  • Caspases
  • Curcumin