FTO-mediates m6A modification enhances ROLLCSC stability. (IMAGE)
Caption
(A) SRAMP analysis of the secondary structure of ROLLCSC and its potential m6A methylation sites. (B) Venn diagram showing methylation-related proteins specifically interacting with the sense strand. (C and D) RIP assay validating the interaction between ROLLCSC and the target protein, with IgG as a negative control. (E) Western blot confirming the specific interaction between ROLLCSC and the target protein. (F) Regulation of ROLLCSC expression by FTO inhibitor. (G) Effect of FTO inhibitor on the stability of the ROLLCSC gene, with ActD concentration at 2 μM. (H) MeRIP analysis of the impact of FTO inhibitor on the m6A methylation level of ROLLCSC. (I) Efficiency of lentiviral overexpression of FTO. (J) Regulation of ROLLCSC expression by lentiviral overexpression of FTO. (K) Effect of lentiviral FTO overexpression on the stability of the ROLLCSC gene, with ActD concentration at 2 μM. (L) MeRIP analysis of the impact of FTO inhibitor on the m6A methylation level of ROLLCSC. (M) Knockdown efficiency of si-Igf2bp2. (N) PCR analysis of the effect of si-Igf2bp2 on ROLLCSC expression. (O) Effect of si-Igf2bp2 on the stability of the ROLLCSC gene, with ActD concentration at 2 μM. (P–Q) Representative images and statistical analysis of transwell assay results for each group. Six randomly selected images per group were used for data analysis. (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. ns, not significant. The results represent three independent experiments.)
Credit
Yu-Han Zhang, Jia-Cheng Xie, Ting Ye, Shi-Meng Guo, Xue Han, Si Yang, Lei Shi, Yi-Shi Li, H. Rosie Xing, Jing-Yu Li, Jian-Yu Wang
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