The present study was designed to observe the expression of the centrosomal protein 63 in papillary thyroid cancer (PTC) tissues and cells and to explore the clinical significance of Cep63 expression in PTC. Primary PTC tissues and matched normal thyroid tissues were collected, and the Cep63 expression level was determined by reverse transcription‑quantitative PCR and western blotting. A stable Cep63‑knockout cell line was constructed to assess the proliferation, invasion, migration and apoptosis abilities in vitro. A subcutaneous tumorigenesis model was established in nude mice to evaluate the effect of Cep63 on tumor growth and proliferation in vivo. Western blotting was used to explore the relevant signaling pathways. The results revealed that the expression level of Cep63 in PTC tissues was significantly increased. The proliferation, invasion and migration abilities of TPC‑1 cells were decreased after Cep63 knockout, and silencing of Cep63 resulted in TPC‑1 cell cycle arrest in the S phase. Mechanistically, Cep63 knockout inhibited the activation of the Janus kinase/signal transducer and activator of transcription 3 signaling pathway. In conclusion, Cep63 knockout significantly inhibited biological functions of TPC‑1 cells in vitro and in vivo, indicating that Cep63 may be an important oncogene of PTC.

中文翻译：

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Cep63 敲除抑制甲状腺乳头状癌细胞系 TPC-1 的恶性表型。

本研究旨在观察中心体蛋白 63 在甲状腺乳头状癌 (PTC) 组织和细胞中的表达，并探讨 Cep63 在 PTC 中表达的临床意义。收集原代PTC组织和匹配的正常甲状腺组织，通过逆转录-定量PCR和蛋白质印迹法测定Cep63的表达水平。稳定Cep63敲除细胞系，构建以评估增殖，侵袭，迁移和凋亡的能力在体外。在裸鼠中建立皮下肿瘤发生模型以评价Cep63对体内肿瘤生长和增殖的影响. 蛋白质印迹被用来探索相关的信号通路。结果显示PTC组织中Cep63的表达水平显着升高。Cep63敲除后TPC-1细胞的增殖、侵袭和迁移能力降低，Cep63的沉默导致TPC-1细胞周期停滞在S期。从机制上讲，Cep63 敲除抑制了 Janus 激酶/信号转导器和转录 3 信号通路激活剂的激活。综上所述，Cep63敲除在体外和体内均显着抑制了TPC-1细胞的生物学功能，表明Cep63可能是PTC的重要致癌基因。