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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

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. 3

Knockdown of VIRMA attenuates the malignant phenotype and enhances sensitivity to cisplatin in vitro. A: CRISPR/Cas9-mediated knockdown of VIRMA in NCCIT cells (~ 50% reduction), leading to decreased protein expression of other members of the writer complex – METTL3, WTAP and METTL14. Results are normalized to ß-actin and expressed as fold-change compared to scramble condition; B: Relative levels of m6A, expressed as fold-change compared to scramble condition, both by ELISA kit (top) and dot blot (bottom, normalized to methylene blue); C – Illustration of the m6A writer complex and hypothesis related to its disruption upon VIRMA knockdown; D – Tumor cell growth curves in VIRMA knockdown cells compared to scramble condition along 72 h; E – Measurement of tumor cell proliferation by BrdU assay along 72 h. Results are expressed as fold-change compared to scramble condition; F – Measurement of migration capacity. Results are expressed as fold-change compared to scramble condition; G - Measurement of invasion capacity. Results are expressed as fold-change compared to scramble condition; H – Cell viability curves for NCCIT-VIRMA knockdown and scramble cells treated with cisplatin. Results are expressed as percentage cells surviving, normalized to the vehicle. IC50 concentration is indicated for each condition. * p < 0.05; ** p < 0.01; **** p < 0.0001

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