ArticleCell death & disease2026
Androgen receptor-dependent DRAM1 activation drives autophagic resistance to BRAF inhibitors in BRAFV600-mutant melanoma.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BRAFV600-mutant melanoma relies on hyperactivation of the MAPK/ERK pathway for tumorigenesis, with BRAF/MEK inhibitors (BRAFi/MEKi) improving patient outcomes. However, therapeutic resistance frequently emerges, and male patients show poorer responses and outcomes, partially linked to androgen receptor (AR) overexpression. Here, we uncover a mechanistic link between AR signaling and autophagic resistance in BRAFV600-mutant melanoma. We show that BRAFi treatment upregulates AR expression, which induces cytoprotective autophagy through transcriptional activation of DRAM1, a key autophagy-related gene. Functional studies reveal that AR-driven autophagy confers resistance to BRAFi by enhancing cellular survival under therapeutic stress. Our findings establish AR-regulated autophagy as a critical resistance mechanism and provide preclinical evidence for combining AR-targeting PROTAC degrader ARV110 with autophagy inhibitors to overcome BRAFi resistance.
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