Fig. 8 | Nature Communications

Fig. 8

From: A requirement for STAG2 in replication fork progression creates a targetable synthetic lethality in cohesin-mutant cancers

Fig. 8The alternative text for this image may have been generated using AI.

STAG2 deficient cancer cells harbor increased sensitivity to cytotoxic chemotherapeutic agents and small molecule inhibitors of DNA double-strand break repair. a Summary of results from chemotherapeutic screen in four pairs of STAG2 isogenic human cells (H4 glioblastoma, 42MGBA glioblastoma, TC-106 Ewing sarcoma, and RPE hTERT shTP53). All four pairs showed similar sensitivities for all agents. b Survival plots of STAG2 isogenic H4 glioblastoma cells following treatment with etoposide (topoisomerase II inhibitor), rucaparib (PARP inhibitor), VX-970 (ATR inhibitor), and panobinostat (HDAC inhibitor). Each data point is the mean of 12 replicates from 3 independent experiments, and error bars show standard error of the mean. Source data are provided as a Source Data file

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