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Fig. 5 | Molecular Cancer

Fig. 5

From: Aberrant m5C hypermethylation mediates intrinsic resistance to gefitinib through NSUN2/YBX1/QSOX1 axis in EGFR-mutant non-small-cell lung cancer

Fig. 5

Epi-transcriptome analysis identifies QSOX1 as an m5C-modified target in resistant NSCLC cells. a, b H1650 cells (a) or PC-9 cells (b) were transfected with siNSUN2 for 72 h or treated with gefitinib (1 µM) for 24 h and the average m5C level was analyzed via RNA-BisSeq. c The m5C distributions within different regions in control, NSUN2 knockdown or gefitinib-treated H1650 cells. d Significant changes in the m5C methylation and mRNA expression levels in H1650 siNSUN2#1 cells. e Venn diagram illustrating the potential m5C modification candidates of direct NSUN2 targets. f, g IGV analysis showed that changes in mRNA expression and m5C levels of QSOX1 in H1650 (f) and PC-9 (g) cells upon NSUN2 knockdown or gefitinib treatment. h-j Purified mRNA was immunoprecipitated by anti-m5C antibody and the m5C levels of QSOX1 in H1650 (h), H1975 (i), and HCC2279 (j) were analyzed by qRT-PCR. Error bars are means ± SD of three independent experiments. ns, not significant, **p < 0.01, ***p < 0.001.

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Molecular Cancer

ISSN: 1476-4598