Moreover, ABCB5-positive cells contribute to the formation of an immunosuppressive microenvironment by secreting cytokines (IL-6, IL-8, TGF-β) and expressing immune checkpoint ligands, such as PD-L1, thereby favoring tumor progression and a poor prognosis. This review integrates current data on the molecular and microenvironmental mechanisms underlying melanoma progression and therapy resistance, and positions ABCB5 within the broader landscape of melanoma resistance mechanisms, emphasizing both its potential and its current limitations as a biomarker and therapeutic target.
Compared with 2D cultures, 3D models better preserved and upregulated key mesenchymal markers (Vimentin and CDH2). Our findings show how these biomimetic 3D platforms better replicate sarcoid TME, offering a promising tool for comparative oncology and PV-related human cancers.
Rare reports of metastasis suggest a potentially more aggressive clinical course than typical BCC. Comprehensive excision and long-term surveillance are recommended to optimize outcomes and further characterize this rare variant.
Using A375 and SK-MEL-28 melanoma cells treated with the ferroptosis inducer erastin, we analyzed USP36 expression and evaluated its functional role through both overexpression and knockdown experiments...Collectively, these findings establish USP36 as an oncogene in melanoma that inhibits ferroptosis through stabilization of APEX1. Therefore, targeting the USP36-APEX1 axis may represent a novel therapeutic approach for melanoma treatment.