Fig. 2
In CC, m6A regulatory proteins contribute to tumorigenesis and metastasis by interacting with various RNAs. piRNA-14633 mimic increases the mRNA stability of METTL14 and CYP1B1 expression levels, leading to the malignancy of CC. METTL3, which is up-regulated by TBP, regulates the glycolysis of CC via the regulation of PDK4. METTL3 promotes/inhibits the tumorigenesis and metastasis of CC by interacting with various RNAs, including E2F1, circ0000069, ZFAS1, miR-193b, FOXD2-AS1, and HK2. FTO and ALKBH5 promote/inhibit the tumorigenesis and metastasis of CC by regulating the expression of β-catenin, HOXC13-AS, E2F1, MYC, and GAS5. circARHGAP12 interacts with IGF2BP2 to enhance the mRNA stability of FOXM1, thereby promoting the proliferation and migration of CC. E6/E7 regulates the aerobic glycolysis of CC cells through the IGF2BP2-mediated modulation of m6A-MYC mRNA. KCNMB2-AS1 and IGF2BP3 form a positive regulatory circuit, which increases the tumorigenic effect of KCNMB2-AS1 in CC. YTHDF1, YTHDF2, and IGF2BP3 promote/inhibit the tumorigenesis and metastasis of CC by regulating the expression levels of GAS5, CTNNB1, ACIN1, PDK4, HK2, and RANBP2