Publications by authors named "M R Shende"
Synovial Sarcoma (SS) is driven by the SS18::SSX fusion oncoprotein and is ultimately refractory to therapeutic approaches. SS18::SSX alters ATP-dependent chromatin remodeling BAF (mammalian SWI/SNF) complexes, leading to the degradation of canonical (cBAF) complex and amplified presence of an SS18::SSX-containing non-canonical BAF (ncBAF or GBAF) that drives an SS-specific transcription program and tumorigenesis. We demonstrate that SS18::SSX activates the SUMOylation program and SSs are sensitive to the small molecule SAE1/2 inhibitor, TAK-981.
View Article and Find Full Text PDFSynovial Sarcoma (SS) is driven by the SS18::SSX fusion oncoprotein. and is ultimately refractory to therapeutic approaches. SS18::SSX alters ATP-dependent chromatin remodeling BAF (mammalian SWI/SNF) complexes, leading to the degradation of canonical (cBAF) complex and amplified presence of an SS18::SSX-containing non-canonical BAF (ncBAF or GBAF) that drives an SS-specific transcription program and tumorigenesis.
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- Triple negative breast cancer (TNBC) is responsible for over 30% of breast cancer deaths, yet it represents only 10-15% of all cases, highlighting a significant challenge in treatment.
- Research using CRISPR/Cas9 screening identified that TNBC cells are particularly sensitive to the depletion of UBA1, a ubiquitin-like modifier activating enzyme.
- The UBA1 inhibitor TAK-243 induces severe ER stress and cell death in TNBC cells, particularly those with high c-MYC levels, showing promise for shrinking tumors and reducing metastasis in both lab models and patient-derived xenografts.
The possible anticancer activity of combination (M + E + F) of metformin (M), efavirenz (E), and fluoxetine (F) was investigated in normal HDF cells and HCT116 human colon cancer cells. Metformin increased cellular FOXO3a, p-FOXO3a, AMPK, p-AMPK, and MnSOD levels in HDFs but not in HCT116 cells. Cellular ATP level was decreased only in HDFs by metformin.
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