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Induction of endoplasmic reticulum stress as a strategy for melanoma therapy: is there a future?

David S Hill1,2,1,2, Penny E Lovat2,2, Nikolas K Haass1,3,4,1,3,4

  • 1The Centenary Institute, Newtown, New South Wales, Australia.

Melanoma Management
|September 8, 2018
PubMed

Insights

Melanoma cells resist apoptosis by activating the unfolded protein response (UPR) and increasing protein folding capacity. Targeting UPR and endoplasmic reticulum (ER) stress offers potential melanoma therapies.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Melanoma cells exhibit resistance to apoptosis.
  • Endoplasmic reticulum (ER) stress can trigger apoptosis.
  • The unfolded protein response (UPR) is a key survival mechanism in cancer cells.

Purpose of the Study:

  • To review how melanoma cells evade ER stress-induced apoptosis.
  • To explore therapeutic strategies targeting ER stress in melanoma.

Main Methods:

  • Literature review of cellular survival mechanisms in melanoma.
  • Analysis of UPR signaling pathways.
  • Examination of therapeutic interventions targeting ER stress.

Main Results:

  • Melanoma cells utilize UPR to resist ER stress-induced apoptosis.
  • Oncogene activation suppresses apoptosis.
  • Upregulation of ER chaperones and BCL-2 family proteins enhances cell survival.

Conclusions:

  • Modulating UPR signaling and inducing ER stress are potential therapeutic strategies for melanoma.
  • Targeting protein folding machinery and ER stress pathways may offer new treatment avenues.
Keywords:
ERGrp78/BiPHSP90IRE1αPDIPERKUPRapoptosisendoplasmic reticulum stressmelanomatargeted therapyunfolded protein response

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