Fig. 8: Methylated reading protein IGF2BP3 enhanced the stability of SQLE mRNA in a m6A-dependent manner. | Cell Death & Disease

Fig. 8: Methylated reading protein IGF2BP3 enhanced the stability of SQLE mRNA in a m6A-dependent manner.

From: Stabilization of SQLE mRNA by WTAP/FTO/IGF2BP3-dependent manner in HGSOC: implications for metabolism, stemness, and progression

Fig. 8

a The WTAP positively regulated the m6A modification of SQLE mRNA. b Overexpression of WTAP enhanced the half-life of SQLE mRNA. c The FTO negatively regulated the m6A modification of SQLE mRNA. d Knockdown of FTO enhanced the half-life of SQLE mRNA. e RIP assays showed the combination of IGF2BP1/2/3 with SQLE mRNA. f, g Knockdown IGF2BP1/2 did not reverse the WTAP-induced m6A level of SQLE mRNA. h Knockdown IGF2BP3 reversed the high m6A level of SQLE mRNA that was caused by WTAP overexpression. i RIP assays showed that the interaction of IGF2BP3 with SQLE mRNA was enhanced in cells with WTAP overexpression compared to the control group. j, k Knockdown IGF2BP1/2 did not reverse the FTO knockdown-induced high m6A level of SQLE mRNA. l Knockdown IGF2BP3 reversed the high m6A level of SQLE mRNA that was caused by FTO knockdown. m RIP assays showed that the interaction of IGF2BP3 with SQLE mRNA was enhanced in cells with FTO knockdown compared to the control group. n Knockdown of IGF2BP3 decreased the half-life of SQLE mRNA. o The m6A modification of SQLE mRNA was installed by the m6A methyltransferases WTAP, reverted by the demethylases FTO, and recognized by m6A binding proteins IGF2BP3. *p < 0.05, **p < 0.01, and ***p < 0.001.

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