Fig. 4From: The component of the m6A writer complex VIRMA is implicated in aggressive tumor phenotype, DNA damage response and cisplatin resistance in germ cell tumorsKnockdown of VIRMA contributes cisplatin sensitivity by impairing DNA repair. A - γH2AX levels in VIRMA knockdown and scramble conditions upon treatment with 1 μM and 3.3 μM cisplatin. Results are computed as fluorescence intensity, normalized to number of cells, and expressed as fold-change; B – Transcript levels of RAD9, GADD45A and GADD45B in VIRMA knockdown and scramble conditions upon treatment with 1 μM and 3.3 μM cisplatin. Results are normalized to GUSB, computed in 2^-ΔΔCt format and expressed as fold-change in VIRMA knockdown compared to scramble condition; C – Protein expression of players involved in homologous recombination and non-homologous end joining DNA repair pathways in VIRMA knockdown and scramble conditions upon treatment with 1 μM and 3.3 μM cisplatin. Results are normalized to ß-actin. Values below each band refer to densitometry as fold-change compared to vehicle in the two independent group conditions (scramble and VIRMA knockdown); D – Related to the blots presented in C, the graphs show plotted the fold-change expression of VIRMA knockdown cells compared to scramble condition, for each concentration. *** p < 0.001Back to article page