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RIP1 protects melanoma cells from apoptosis induced by BRAF/MEK inhibitors

Fu Xi Lei1,2, Lei Jin2, Xiao Ying Liu2,3

  • 1Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, 710061, China.

Cell Death & Disease
|June 9, 2018
PubMed

Insights

Receptor-interacting protein kinase 1 (RIP1) promotes melanoma resistance to BRAF/MEK inhibitors by activating NF-κB. Targeting RIP1 alongside these inhibitors may improve melanoma treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Receptor-interacting protein kinase 1 (RIP1) is known to regulate apoptosis and necrosis.
  • The role of RIP1 in promoting cancer cell survival, particularly in melanoma, is not well understood.

Purpose of the Study:

  • To investigate the role of RIP1 in melanoma cell survival and resistance to BRAF/MEK inhibitors.
  • To elucidate the mechanisms by which RIP1 contributes to drug resistance in melanoma.

Main Methods:

  • Analysis of RIP1 expression in melanoma cells.
  • Investigating the involvement of RIP1 in NF-κB activation.
  • Assessing the impact of RIP1 inhibition on melanoma cell survival under drug treatment.
  • Studying the role of Snail1 and CYLD in regulating RIP1 expression.

Main Results:

  • RIP1 is upregulated in melanoma cells and contributes to resistance against BRAF/MEK inhibitors via NF-κB activation.
  • Snail1-mediated suppression of CYLD is critical for RIP1 upregulation upon ERK activation, especially in acquired resistance.
  • RIP1's kinase activity is not essential for mediating NF-κB activation and cell survival during BRAF/MEK inhibition.

Conclusions:

  • RIP1 plays a significant role in both intrinsic and acquired resistance of melanoma to BRAF/MEK inhibitors.
  • Targeting RIP1 in combination with BRAF/MEK inhibitors presents a promising therapeutic strategy for melanoma treatment.

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