Fig 2: Kaplan–Meier survival plots for MED7 nuclear expression: a MED7 vs BCSS in all cases; b MED7 vs BCSS in Luminal A; c MED7 vs BCSS in Luminal B; d MED7 vs BCSS in TPN; e MED7 vs BCSS in HER2+; f MED7 vs MFI in all cases, and g targeted prognostic analyses for MED7 via the BC gene miner in ER+ node-negative patients using Breast Cancer Gene-Expression Miner v4.0

Fig 3: MED12 depletion promotes TGFβ-dependent fork protection in BRCA-deficient cells. (A–C) DNA fiber combing assays showing that MED12 knockdown, but not knockdown of MED7 or CDK8, suppresses HU-induced nascent strand degradation in HeLa-BRCA2KO (A), DLD1-BRCA2KO (B) and RPE1-BRCA1KO (C) cells. Co-depletion of TGFBR2 restores fork degradation in MED12-depleted BRCA1/2-knockout cells, indicating that activation of the TGFβ pathway upon MED12 depletion is essential for fork stability. Knockdown of ZRANB3, which suppresses fork reversal, is shown as control. For all panels, the ratio of CldU to IdU tract lengths is presented, with the median values marked on the graph and listed at the top. At least 100 tracts were quantified for each sample. Asterisks indicate statistical significance (Mann-Whitney test). Schematic representations of the assay conditions are shown at the top. (D) BrdU alkaline comet assay showing that MED12 depletion reduces replication-associated ssDNA gaps accumulation upon HU treatment in HeLa-BRCA2KO cells. At least 75 nuclei were quantified for each condition. The median values are marked on the graph and listed at the top. Asterisks indicate statistical significance (Mann-Whitney test). Schematic representations of the assay conditions are shown at the top.