Results 71 to 80 of about 39,389 (304)
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon +13 more
wiley +1 more source
Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla +10 more
wiley +1 more source
Regulation of Rad52-dependent replication fork recovery through serine ADP-ribosylation of PolD3
Although Poly(ADP-ribose)-polymerases (PARPs) are key regulators of genome stability, how site-specific ADP-ribosylation regulates DNA repair is unclear.
Frederick Richards +7 more
doaj +1 more source
Single circulating tumor cells (sCTCs) from high‐grade serous ovarian cancer patients were enriched, imaged, and genomically profiled using WGA and NGS at different time points during treatment. sCTCs revealed enrichment of alterations in Chromosomes 2, 7, and 12 as well as persistent or emerging oncogenic CNAs, supporting sCTC identity.
Carolin Salmon +9 more
wiley +1 more source
Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon +4 more
wiley +1 more source
CAF‐mediated immunosuppression in ovarian cancer is driven by IDO1, reducing T‐cell function. Inhibiting IDO1 restores T‐cell proliferation and cytotoxicity, increases cancer cell apoptosis, and may help overcome CAF‐induced immune suppression in high‐grade serous ovarian cancer. Targeting IDO1 may improve antitumor immunity.
Hyewon Lee +3 more
wiley +1 more source
Basal Activity of a PARP1-NuA4 Complex Varies Dramatically across Cancer Cell Lines
Poly(ADP-ribose) polymerases (PARPs) catalyze poly(ADP-ribose) addition onto proteins, an important posttranslational modification involved in transcription, DNA damage repair, and stem cell identity.
Kristin A. Krukenberg +3 more
doaj +1 more source
We analyzed alterations of PAR metabolism‐related proteins in PARG inhibitor‐resistant HCT116RPDD cells. Although PARG levels remained unchanged, HCT116RPDD cells exhibited reduced PARP1 and ARH3 expression and elevated PAR levels. Interestingly, HCT116RPDD cells exhibited slightly elevated intracellular NAD+/NADH and ATP levels. Our findings suggest a
Kaede Tsuda, Yoko Ogino, Akira Sato
wiley +1 more source
Poly(ADP-ribosyl)ation is required to modulate chromatin changes at c-MYC promoter during emergence from quiescence. [PDF]
Poly(ADP-ribosyl)ation is a post-translational modification of various proteins and participates in the regulation of chromatin structure and transcription through complex mechanisms not completely understood.
Cassandra Mostocotto +5 more
doaj +1 more source
Poly(ADP-ribose) Binds to Specific Domains in DNA Damage Checkpoint Proteins*
Poly(ADP-ribose) is formed in possibly all multicellular organisms by a familiy of poly(ADP-ribose) polymerases (PARPs). PARP-1, the best understood and until recently the only known member of this family, is a DNA damage signal protein catalyzing its ...
J. Pleschke +3 more
semanticscholar +1 more source

