Etoposide-Generated Live Melanoma Cells Upregulate B2M and Lose Tumor-Forming Ability
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A preprint posted on bioRxiv in Cancer Biology on October 20, 2026, reports that live immunogenic melanoma cells generated by etoposide treatment upregulate B2M and lose tumor-forming potential. After etoposide washout, the live fraction of treated B16-Ova melanoma cells is growth-arrested but remains viable, and a soft-agar colony-formation assay shows a near-complete loss of anchorage-independent growth. The treated cells upregulate B2M, a Class I MHC subunit, but immunofluorescence shows the protein accumulates mainly in a perinuclear intracellular pattern with no enhanced surface staining, and western blotting shows only a marginal increase in Class I MHC expression. How the intracellular B2M localization relates to the cells' lost tumor-forming potential remains unresolved.
Written by a model from the reports · updated 3 hours ago
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- bioRxivPickLive immunogenic melanoma cells generated by etoposide treatment upregulate B2M and lose tumor-forming potential
In etoposide-treated B16-Ova melanoma cells, the live fraction is growth-arrested after drug washout but remains viable, and soft-agar colony-formation assays show a near-complete loss of anchorage-independent growth. Treated cells upregulate production of B2M (Beta-2-microglobulin, a Class I MHC subunit), but immunofluorescence shows B2M mainly accumulates in the perinuclear intracellular region with no enhanced surface staining, and western blot shows only a marginal increase in Class I MHC expression.
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