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MST1 activation by curcumin mediates JNK activation, Foxo3a nuclear translocation and apoptosis in melanoma cells

Teng Yu1, Jiang Ji, Yong-li Guo

  • 1Department of Dermatology, Shandong Ji-ning No. 1 People's Hospital, Shandong Province 272011, PR China.

Biochemical and Biophysical Research Communications
|October 19, 2013
PubMed

Insights

Curcumin triggers melanoma cell death by activating mammalian Sterile 20-like kinase 1 (MST1). This pathway involves reactive oxygen species (ROS) and c-Jun N-terminal protein kinase (JNK), leading to apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Curcumin is known to induce apoptosis in melanoma cells.
  • The precise molecular mechanisms underlying curcumin's pro-apoptotic effects in melanoma require further elucidation.
  • The role of mammalian Sterile 20-like kinase 1 (MST1) in this process has not been fully explored.

Purpose of the Study:

  • To investigate the role of mammalian Sterile 20-like kinase 1 (MST1) in curcumin-induced apoptosis of melanoma cells.
  • To determine the involvement of reactive oxygen species (ROS) and c-Jun N-terminal protein kinase (JNK) in this pathway.
  • To explore the downstream targets of MST1 activation by curcumin.

Main Methods:

  • Melanoma cell culture and treatment with curcumin.
  • MST1 silencing using RNA interference (RNAi).
  • Assessment of apoptosis, ROS production (using N-acetyl-cysteine (NAC) as a scavenger), MST1 activation, JNK activation, Foxo3 nuclear translocation, and Bim-1 expression.

Main Results:

  • Curcumin activated MST1, leading to apoptosis in melanoma cells.
  • MST1 silencing reduced curcumin-induced apoptosis, while MST1 overexpression enhanced sensitivity.
  • Curcumin-induced ROS production was essential for MST1 activation.
  • JNK activation, Foxo3 nuclear translocation, and Bim-1 expression were dependent on MST1 activation by curcumin.

Conclusions:

  • MST1 activation is a key mediator of curcumin-induced apoptosis in melanoma cells.
  • The pathway involves ROS generation, MST1 activation, subsequent JNK activation, and Foxo3a nuclear translocation, ultimately promoting apoptosis.
  • These findings highlight MST1 as a potential therapeutic target in melanoma treatment.
Keywords:
3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl tetrazolium bromideApoptosisCurcuminIPJNKJNK and Foxo3aMST1MTTMelanomaN-acetyl-cysteineNACRNA interferenceRNAiROSc-Jun N-terminal protein kinaseimmunoprecipitationmammalian Sterile 20-like kinase 1reactive oxygen species

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