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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: The component of the m6A writer complex VIRMA is implicated in aggressive tumor phenotype, DNA damage response and cisplatin resistance in germ cell tumors

Fig. 4

Knockdown 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 < 0.001

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