Fig. 5: CtBP1/2 KD significantly increased DNA repair response to chemotherapy drug. | Oncogenesis

Fig. 5: CtBP1/2 KD significantly increased DNA repair response to chemotherapy drug.

From: CtBP1/2 differentially regulate genomic stability and DNA repair pathway in high-grade serous ovarian cancer cell

Fig. 5

The cell survival comparison between CtBP1/2 KD and control the response to DNA-PK inhibitor NU7441 (A) and KU treatment (B). Immunofluorescence of gH2AX and RPA32 phosphorylation detected in control and CtBP1/2 KD cells after cell treated with ENA-PK inhibitor NU7441 and KU000487. Nuclear DNA was counterstained with DAPI (C). Quantitative analysis foci formation per cell in each group was performed by Image J and presented as γH2AX foci/cell (D) and RPA32 foci/cell (E). *P < 0.05; **P < 0.001. The contribution of CtBP1/2 in the regulation of balance shifted between homology-dependent vs. homology-independent repair model in ovarian cancer cells (F). The SeeSaw 2.0 reporter was employed to detect the balance shift between homology-dependent vs. homology-independent repair among CtBP1/2 knockdown and control cells in rest condition, treated with carboplatin and etoposide. To measure the deviation from the balance between NHEJ and HR, the ratio between green vs. red cells in each condition was calculated. To facilitate comparing experiments, this ratio was normalized shRNA control. Those skewed the balance towards an increase in homology-independent repair has a fold-increase of over 1, while those with an increase in HR have a fold-decrease of less than one. Data represent a minimum of three sets of duplicated experiments. Western blot analyzed the key regulators between CtBP1/2 knockdown and control (G). Rest represents without stimulation.

Back to article page