UBE2T Enhances Thyroid Papillary Carcinoma Proliferation through Fine-Tuned JAK-STAT Pathway Regulation
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Department of General Surgery, The First Affiliated Hospital with Nanjing Medical University

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    Abstract:

    Objective: This study aims to investigate the expression of Ubiquitin-Binding Enzyme E2T (UBE2T) in Papillary Thyroid Carcinoma (PTC) and its impact on patient prognosis. Additionally, we explore UBE2T's direct effects on PTC cell biology, aiming to identify potential regulatory pathways and provide theoretical foundations for future targeted therapies. Methods: Utilizing The Cancer Genome Atlas (TCGA) database, we systematically analyzed UBE2T expression in PTC and its correlation with patient prognosis. Western blotting (WB) assessed UBE2T expression in thyroid normal and tumor tissues. UBE2T knockdown experiments were conducted in PTC cell lines (TPC-1, KTC-1) using CCK-8, colony formation, Transwell, and scratch assays to evaluate proliferation, migration, and invasion abilities, with WB measuring protein level changes.Results: TCGA analysis revealed significantly elevated UBE2T in PTC tissues, correlating with disease-free interval and lymph node metastasis (P <0.01). UBE2T knockdown led to decreased proliferation, inhibited invasion and migration in TPC-1 and KTC-1 cells, accompanied by reduced STAT phosphorylation. Adding a STAT activator in UBE2T-knockdown cells significantly increased proliferation without significant changes in invasion and migration. Conclusion: UBE2T knockdown suppresses proliferation, migration, and invasion in PTC cell lines, suggesting UBE2T as a potential therapeutic target for PTC by modulating the JAK-STAT signaling pathway.

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History
  • Received:February 06,2024
  • Revised:March 22,2024
  • Adopted:May 22,2024
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