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Additional file 5: of METTL3 facilitates tumor progression via an m6A-IGF2BP2-dependent mechanism in colorectal carcinoma

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posted on 2019-06-24, 05:00 authored by Ting Li, Pei-Shan Hu, Zhixiang Zuo, Jin-Fei Lin, Xingyang Li, Qi-Nian Wu, Zhan-Hong Chen, Zhao-Lei Zeng, Feng Wang, Jian Zheng, Demeng Chen, Bo Li, Tie-Bang Kang, Dan Xie, Dongxin Lin, Huai-Qiang Ju, Rui-Hua Xu
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)

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National Natural Science Foundation of China

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