Northwestern Medicine researchers have identified a significant pathway in B-cell lymphomas involving BAP1, an enzymatic subunit implicated in tumor suppression. BAP1's dual roles as both a potential tumor suppressor and oncogene are explored in this study. BAP1 enhances the expression of MHC-II genes, critical for immune function. The study shows that depleting BAP1 in lymphoma cells decreases immune cell infiltration and promotes tumor growth. Inhibition of the PRC1 complex can restore MHC-II expression in BAP1-deficient cells, suggesting therapeutic avenues for enhancing immune response in B-cell lymphoma.
Some scientists believe that BAP1, the enzymatic subunit within the PR-DUB complex, is a tumor suppressor because loss of BAP1 was observed in some specific tumor types.
In the current study, investigators analyzed multiple cultured human cancer cell lines with BAP1 and compared them to cell lines that had BAP1 inhibited.
They found depletion of the BAP1 gene in B-cell lymphoma cells reduced immune cell infiltration and accelerated tumor growth in animal models.
Investigators inhibited PRC1, which antagonizes BAP1 activity, and found that it restored MHC-II expression in BAP1-deficient lymphoma cells.
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