Role of the SEC62 gene in dermato‐oncology – impact on tumor cell biology, prognostication, and personalized therapy management

Summary The SEC62 gene encodes for a transmembrane protein of the endoplasmic reticulum (ER). Sec62 protein is involved in the post‐translational transport of secretory and membrane‐bound proteins in eukaryotic cells, regulates intracellular calcium homeostasis through direct interaction with the Se...

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Veröffentlicht in:Journal der Deutschen Dermatologischen Gesellschaft 2022-09, Vol.20 (9), p.1187-1199
Hauptverfasser: Linxweiler, Maximilian, Müller, Cornelia S. L.
Format: Artikel
Sprache:eng
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Zusammenfassung:Summary The SEC62 gene encodes for a transmembrane protein of the endoplasmic reticulum (ER). Sec62 protein is involved in the post‐translational transport of secretory and membrane‐bound proteins in eukaryotic cells, regulates intracellular calcium homeostasis through direct interaction with the Sec61 channel and makes a decisive contribution to the cellular compensation of ER stress in the context of recovER‐phagy. A significantly increased expression of the SEC62 gene has already been demonstrated in various tumor entities. First approaches of a targeted therapy have been tested for various tumor entities in vitro and in vivo with promising results that motivate further preclinical and clinical studies. Nevertheless, many questions remain unanswered, in particular with regard to the molecular mechanisms underlying the observed clinical effects, and require further investigation in future studies. The protein also plays a relevant role in dermato‐oncology. The overexpression of SEC62 in atypical fibroxanthomas and malignant melanomas has already been demonstrated and a correlation of SEC62 expression with various clinical and pathological features has been observed. Future studies, especially in vivo and clinical, will show whether Sec62 can be established as a prognostic marker in dermato‐oncology and whether it can serve as a starting point for targeted therapy.
ISSN:1610-0379
1610-0387
DOI:10.1111/ddg.14817