Department of Pathology, Pingshan District People's Hospital of Shenzhen, Pingshan General Hospital of Southern Medical University, Shenzhen 518118, China.
Department of Pathology, Pingshan District People's Hospital of Shenzhen, Pingshan General Hospital of Southern Medical University, Shenzhen 518118, China.
Tissue Cell. 2023 Oct;84:102193. doi: 10.1016/j.tice.2023.102193. Epub 2023 Aug 9.
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/β-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/β-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/β-catenin signaling pathway.
甲状腺癌的发病率在全球范围内不断上升，尤其是在女性中。研究表明，ANKRD22 在多种癌症中异常激活，但尚不清楚其在甲状腺乳头状癌（PTC）中是否也高度表达。我们的目的是评估 ANKRD22 在 PTC 中的作用。通过癌症基因组图谱验证了 ANKRD22 在组织中的表达存在差异，并进一步通过肿瘤免疫估计资源进行了预测。通过聚合酶链反应和蛋白质印迹检测预测结果。随后，通过 RNA 干扰抑制 ANKRD22 在细胞中的表达，并结合细胞计数试剂盒-8 测定、Transwell 测定和集落形成测定来检查细胞进展的变化。最后，通过蛋白质印迹研究了 ANKRD22 敲低对上皮-间充质转化和 Wnt/β-连环蛋白信号通路的影响。通过建立体内小鼠模型来验证 ANKRD22 的作用。本研究发现，ANKRD22 在 PTC 中高表达，这通过聚合酶链反应和蛋白质印迹得到了验证。ANKRD22 的敲低显著降低了细胞活力、集落形成能力以及细胞侵袭和迁移能力。此外，我们发现，ANKRD22 的敲低损害了肿瘤上皮-间充质转化和 Wnt/β-连环蛋白信号通路的激活。总之，本研究揭示了敲低 ANKRD22 通过调节 Wnt/β-连环蛋白信号通路抑制甲状腺乳头状癌细胞的生长和迁移。
