MFN2 Stabilization: A Bridge for Endoplasmic Reticulum Stress Sensitivity in Melanoma

Charles H Adelmann; Inbal Rachmin; David E Fisher

doi:10.1016/j.jid.2021.05.003

MFN2 Stabilization: A Bridge for Endoplasmic Reticulum Stress Sensitivity in Melanoma

J Invest Dermatol. 2021 Dec;141(12):2782-2784. doi: 10.1016/j.jid.2021.05.003. Epub 2021 Sep 23.

Authors

Charles H Adelmann¹, Inbal Rachmin¹, David E Fisher²

Affiliations

¹ Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
² Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. Electronic address: dfisher3@partners.org.

PMID: 34565559
DOI: 10.1016/j.jid.2021.05.003

Abstract

In a new article in the Journal of Investigative Dermatology, Wang et al. (2021) report that mitochondrial quality control modulates responses to endoplasmic reticulum (ER) stress in melanoma. They implicate a linear pathway of XBP1, MARCH5, and MFN2 that act together to regulate mitochondrial fission and mitophagy and ultimately mediate melanoma cell sensitivity to ER stress. This work informs therapeutic combinations and biomarker strategies for targeting melanoma organellar homeostasis as well as for life‒death decisions.

Publication types

Comment

MeSH terms

Endoplasmic Reticulum / metabolism
Endoplasmic Reticulum Stress*
GTP Phosphohydrolases / genetics
GTP Phosphohydrolases / metabolism
Humans
Melanoma* / metabolism
Mitochondria
Mitochondrial Proteins / metabolism
Mitophagy

Substances

Mitochondrial Proteins
GTP Phosphohydrolases
MFN2 protein, human