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Biology subjects

Paradkar, S.

Publications and source records attributed to Paradkar, S..

2 recordsLinked to original sources

PARG inhibition induces nuclear aggregation of PARylated PARP1

PARG inhibitors are currently under clinical development for the treatment of DNA repair-deficient cancers, however, their precise mechanism of action is still unclear. Here we report that PARG inhibition causes increased nuclear PARylated PARP1 that limits PARP1 chromatin binding in response to DNA damage. This PARylated PARP1 accumulates as aggregates at sites distinct from the site of DNA damage, leading to the mis-localization of PARP1. Additionally, these aggregates are formed through PAR chains as abrogating PARP1 catalytic activity prevents their formation. Finally, these PARP1 nuclear aggregates persist long-term and are associated with cleaved cytoplasmic PARP1, a cell death hallmark, which ultimately leads to a non-apoptotic form of cell death. Overall, our data uncovers a novel mechanism of PARG inhibitor cytotoxicity, which will inform ongoing clinical studies.

cancer biology↗

Setdb1-loss induces type-I interferons and immune clearance of melanoma

Despite recent advances in the treatment of melanoma, many patients with metastatic disease still succumb to their disease. To identify tumor-intrinsic modulators of immunity to melanoma, we performed a whole-genome CRISPR screen in melanoma and identified multiple components of the HUSH complex, including Setdb1, as hits. We found that loss of Setdb1 leads to increased immunogenicity and complete tumor clearance in a CD8+ T-cell dependent manner. Mechanistically, loss of Setdb1 causes de-repression of endogenous retroviruses (ERVs) in melanoma cells and triggers tumor-cell intrinsic type-I interferon signaling, upregulation of MHC-I expression, and increased CD8+ T-cell infiltration. Furthermore, spontaneous immune clearance observed in Setdb1-/- tumors results in subsequent protection from other ERV-expressing tumor lines, supporting the functional anti-tumor role of ERV-specific CD8+ T-cells found in the Setdb1-/- microenvironment. Blocking the type-I interferon receptor in mice grafted with Setdb1-/- tumors decreases immunogenicity by decreasing MHC-I expression, leading to decreased T-cell infiltration and increased melanoma growth comparable to Setdb1wt tumors. Together, these results indicate a critical role for Setdb1 and type-I interferons in generating an inflamed tumor microenvironment, and potentiating tumor-cell intrinsic immunogenicity in melanoma. This study further emphasizes regulators of ERV expression and type-I interferon expression as potential therapeutic targets for augmenting anti-cancer immune responses.

cancer biology↗