UBE2T promotes PTC progression by activating the JAK/STAT3 pathway via negative regulation of SOCS2

Background Thyroid cancer, particularly papillary thyroid carcinoma (PTC), is one of the most common malignant tumors of the endocrine system. Malignant biological behaviors such as tumor invasion and cervical lymph node metastasis are closely associated with the prognosis of PTC. To date, no effective method has been identified to accurately predict the invasive biological behavior of PTC. Objective This study aims to investigate the potential molecular mechanisms underlying the high invasiveness of PTC mediated by UBE2T. Methods We examined the expression of UBE2T in PTC using data from the TCGA and GEO databases and validated these findings in clinical samples from our institution, analyzing clinical pathological features. Subsequently, we explored the impact of UBE2T on the biological behavior of PTC cells through stable overexpression or knockdown of the UBE2T gene. Additionally, we elucidated the potential mechanisms by which UBE2T promotes PTC progression, with a particular focus on its role in activating the JAK-STAT signaling pathway. Results Our results demonstrate that UBE2T plays a crucial role in promoting PTC progression by activating the JAK-STAT signaling pathway. Correlation analysis and co-immunoprecipitation (co-IP) experiments identified cytokine signaling suppressor 2 (SOCS2) as a key molecule mediating UBE2T's action in the JAK-STAT pathway. Further rescue experiments and immunofluorescence (IF) assays confirmed that UBE2T promotes PTC progression by negatively regulating SOCS2, thereby activating the JAK-STAT3 pathway. Conclusion This study reveals the mechanistic role of UBE2T in the high invasiveness of PTC, highlighting its negative regulation of SOCS2 to activate the JAK-STAT3 signaling pathway and drive PTC progression. These findings provide new insights into the mechanisms of PTC invasion and may offer potential therapeutic targets for inhibiting PTC metastasis and recurrence.