N6-methylation (m6A) modifications are acknowledged as the most ubiquitous chemical alterations in eukaryotic mRNA, significantly influencing cancer progression. Nonetheless, the precise roles of IGF2BP2 in papillary thyroid carcinoma (PTC) remain little understood. We observed an upregulation of IGF2BP2 in PTC. Functionally, IGF2BP2 enhanced the proliferation, migration and invasion of PTC cells in vitro , and accelerated cancer progression in vivo . Mechanistically, IGF2BP2 facilitated the advancement of PTC towards malignancy by activating the MAPK/MEK/ERK pathway and identifying the m6A alteration in SPRY1 mRNA. Simultaneously, SPRY1 is essential in the carcinogenesis of PTC. Additionally, the TGF-β/SMAD4 pathway enhanced IGF2BP2 expression. Our findings suggest that the TGF-β/SMAD4 pathway facilitates tumorigenesis and malignant progression of PTC by activating the IGF2BP2/SPRY1/MEK/ERK pathway. This may aid in the evaluation and treatment of PTC.
Zeng et al. (Sun,) studied this question.