%0 Figure %A Li, Ting %A Hu, Pei-Shan %A Zuo, Zhixiang %A Lin, Jin-Fei %A Li, Xingyang %A Wu, Qi-Nian %A Chen, Zhan-Hong %A Zeng, Zhao-Lei %A Wang, Feng %A Zheng, Jian %A Chen, Demeng %A Li, Bo %A Kang, Tie-Bang %A Xie, Dan %A Lin, Dongxin %A Ju, Huai-Qiang %A Xu, Rui-Hua %D 2019 %T Additional file 5: of METTL3 facilitates tumor progression via an m6A-IGF2BP2-dependent mechanism in colorectal carcinoma %U https://springernature.figshare.com/articles/figure/Additional_file_5_of_METTL3_facilitates_tumor_progression_via_an_m6A-IGF2BP2-dependent_mechanism_in_colorectal_carcinoma/8312921 %R 10.6084/m9.figshare.8312921.v1 %2 https://springernature.figshare.com/ndownloader/files/15576584 %K Colorectal cancer %K N6-methyladenosine (m6A) %K METTL3 %K SOX2 %K IGF2BP2 %X Figure S2, related to Fig. 2: Identification of METTL3 targets via MeRIP-seq and RNA-seq. a, Volcano Plots showing the numbers of transcripts with significantly increased and decreased m6A peaks (fold change > 1.5 or < − 1.5, P < 0.05) in SW620 cells compared with SW480 cells (left) and in METTL3-knockdown SW620 compared with the control SW620 cells (right). b, Venn diagram showing the shared peaks between metastatic-related hyper-methylated peaks with METTL3-related hypo-methylated peaks. c, Gene-specific m6A qPCR analysis of alterations in the m6A level in four representative genes in METTL3 knockdown HCT116 compared with the control cells. d, Real-time PCR analysis of mRNA expression of four representative genes in METTL3 knockdown and control SW620 and HCT116. The data in c, and d are presented as the means ± SDs (n = 3). *P < 0.05, **P < 0.01 (Student’s t-test). The relative m6A level was normalized by input. The relative expression level was normalized by β-Actin. (TIF 6844 kb) %I figshare