Bioinformatic identification reveals a m6A-binding protein, IGF2BP2, as a novel tumor-promoting gene signature in thyroid carcinoma.

N6-methyladenosine (m6A) modification plays a crucial role in thyroid carcinoma (THCA). Insulin-like growth factor 2 binding protein 2 (IGF2BP2) is a m6A-binding protein. We aimed to explore the effect of IGF2BP2 on the development of THCA. Differentially expressed genes (DEGs) were screened from GSE50901 and GSE60542 datasets. LinkedOmics, Genebank, and Sequence-based RNA Adenosine Methylation Site Predictor databases were employed to find potential m6A modification sites. Protein-protein interaction network and receiver-operating characteristic curves were applied to determine hub genes of THCA. ESTIMATE revealed the effect of IGF2BP2 on tumor immunity. The mRNA expression of IGF2BP2 was detected using real-time quantitative polymerase chain reaction. The viability, migration, and invasion were assessed by Cell Counting Kit-8, wound healing, and transwell assays. A total of 166 common DEGs were identified from GSE50901 and GSE60542 datasets. One m6A-related gene, IGF2BP2, was differentially expressed in THCA and selected as the research target. The hub genes (CD44, DCN, CXCL12, ICAM1, SDC4, KIT, CTGF, and FMOD) were identified with high prediction values for THCA. Subsequently, the target genes of IGF2BP2, SDC4, and ICAM1, which had potential m6A modification sites, were screened out based on the hub genes. IGF2BP2 was upregulated in THCA and IGF2BP2 expression was positively correlated with immune infiltration in THCA. Additionally, knockdown of IGF2BP2 inhibited the proliferation, invasion, and migration of THCA cells. IGF2BP2 has a contributory effect on the progression of THCA, which is a novel biomarker and a therapeutic target for THCA.