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Loss of Concurrent Regulation of the Expression of BIF-1, BAX, and Beclin-1 in Primary and Metastatic Melanoma

Ž. Frangež1, S. M. Seyed Jafari2, R. E. Hunger2, and H.-U. Simon1,3,a*

1Institute of Pharmacology, University of Bern, 3010 Bern, Switzerland

2Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland

3Department of Clinical Immunology and Allergology, Sechenov University, 119435 Moscow, Russia

* To whom correspondence should be addressed.

Received July 8, 2020; Revised July 8, 2020; Accepted July 12, 2020
Melanoma is one of the most aggressive and drug-resistant cancers. Despite novel promising therapeutic strategies, the prognosis of metastatic melanoma patients remains poor and it is often associated with high relapse rates. Endophilin B1, also known as BIF-1, is a multifunctional protein involved in several biological processes such as autophagy and apoptosis. BIF-1 promotes apoptosis through binding to BAX and its translocation to the mitochondrial outer membrane. On the other hand, BIF-1 can interact with Beclin-1 through UVRAG to promote autophagy. Several reports suggest an ambiguous role of BIF-1 in cancer development and progression. For example, it has been demonstrated that the expression of BIF-1 is reduced in both primary and metastatic melanoma and that the reduction of BIF-1 expression is associated with reduced overall survival of melanoma patients. Here we show that the expression of Beclin-1 and active form of BAX are also reduced in the melanoma patients. However, while we observed strong positive correlations between the expression of BIF-1 and Beclin-1 as well as between BIF-1 and BAX in benign nevi, these correlations were lost in the primary and metastatic melanoma cells. These data indicate disruption in the proximal molecular mechanisms which regulate expression of BIF-1, Beclin-1, and BAX in the primary and metastatic melanoma.
KEY WORDS: apoptosis, autophagy, BAX, Beclin-1, BIF-1, melanoma

DOI: 10.1134/S0006297920100107