Published online Nov 20, 2015. doi: 10.5493/wjem.v5.i4.206
Peer-review started: March 28, 2015
First decision: May 13, 2015
Revised: July 29, 2015
Accepted: September 7, 2015
Article in press: September 8, 2015
Published online: November 20, 2015
Melanoma is the most aggressive form of skin cancer. Disrupted intracellular signaling pathways are responsible for melanoma's extraordinary resistance to current chemotherapeutic modalities. The pathophysiologic basis for resistance to both chemo- and radiation therapy is rooted in altered genetic and epigenetic mechanisms that, in turn, result in the impairing of cell death machinery and/or excessive activation of cell growth and survival-dependent pathways. Although most current melanoma therapies target mitochondrial dysregulation, there is increasing evidence that endoplasmic reticulum (ER) stress-associated pathways play a role in the potentiation, initiation and maintenance of cell death machinery and autophagy. This review focuses on the reliability of ER-associated pathways as therapeutic targets for melanoma treatment.
Core tip: This editorial describes the clinical validity of the endoplasmic reticulum (ER) as therapeutic target for melanoma treatment. In addition, we highlight in this review the mechanistic role of ER stress in the modulation of both apoptosis and autophagy- associated pathways. Drugs that perturb ER function may represent an alternative approach for melanoma treatment. This paper reviews the pervious and current published studies on the reliability of ER-associated pathways as therapeutic targets for melanoma.