ANKRD22 knockdown suppresses papillary thyroid cell carcinoma growth and migration and modulates the Wnt/ß-catenin signaling pathway.

The incidence of thyroid cancer is escalating globally, particularly among women. Studies have demonstrated the abnormal activation of Ankyrin Repeat Domain 22 (ANKRD22) in various cancers, but it remains uncertain whether it is also highly expressed in papillary thyroid carcinoma (PTC). Our objective was to evaluate the role of ANKRD22 in PTC. The expression of ANKRD22 varies among tissues, as validated by the Cancer Genome Atlas, and further predicted using the Tumor Immune Estimation Resource. Predicted results were examined via polymerase chain reaction and western blotting. Subsequently, the expression of ANKRD22 in cells was suppressed by RNA interference, and changes in cell progression were examined in conjunction with the cell counting kit-8 assay, transwell assay, and colony formation assay. Finally, the effects of ANKRD22 knockdown on the Epithelial-to-Mesenchymal transition and the Wnt/ß-catenin signaling pathway were investigated through western blotting. An in vivo mice model was established to validate the effect of ANKRD22. This study discovered that ANKRD22 was highly expressed in PTC, which was validated by polymerase chain reaction and western blotting. Knockdown of ANKRD22, significantly reduced thecell viability, colony formation capability, and cell invasion and migration abilities. Furthermore, we found that knockdown of ANKRD22 impaired both tumor Epithelial-to-Mesenchymal transition and the activation of the Wnt/ß-catenin signaling pathway. In conclusion, this study revealed that the knockdown of ANKRD22 inhibits the growth and migration of papillary thyroid cell carcinoma by regulating the Wnt/ß-catenin signaling pathway.