Fig. 7: KRAS contributes to ALKBH8-mediated CRC progression.

a Immunoblotting analysis of control cells and KRAS knockdown cells. b Cell cycle analysis of control cells and KRAS knockdown cells. c Statistical analysis of cell cycle distribution in (b). Mean ± SEM, 3 biological replicates, one-way ANOVA with Dunnett’s multiple comparisons test. d Immunoblotting analysis of control cells and A8-KO cells with or without KRAS overexpression. e Cell cycle analysis of control cells and A8-KO cells with or without KRAS overexpression. f Statistical analysis of cell cycle distribution in (e). Mean ± SEM, 3 biological replicates, one-way ANOVA with Tukey’s multiple comparisons test. g The volume of xenograft tumors from mice implanted with control cells and A8-KO cells with or without KRAS expression. Mean ± SEM. 5 mice for each group, one-way ANOVA with Tukey’s multiple comparisons test. h The images of xenograft tumors from mice implanted with control cells and A8-KO cells with or without KRAS expression. i The analysis of tumor weight in (h). Mean ± SEM, 5 mice for each group, one-way ANOVA with Tukey’s multiple comparisons test. j Representative immunohistochemistry (IHC) images depicting KRAS protein level and ALKBH8 protein level in adjacent normal tissue and CRC tissue in a CRC tissue array. k IHC scoring of ALKBH8 and KRAS in para-cancer tissues and CRC tissues. Distribution of low (+) and high (++) levels of ALKBH8 and KRAS protein expression in para-cancer tissues and CRC tissues. Two-sided Chi-square test; n = 80 for each group. l Two-sided Pearson’s correlation showed relationship of ALKBH8 and KRAS by using H-score. n = 80. Source data are provided as a Source Data file.