Department of Thyroid Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Oncol Rep. 2021 Sep;46(3). doi: 10.3892/or.2021.8150. Epub 2021 Jul 23.
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 . A subcutaneous tumorigenesis model was established in nude mice to evaluate the effect of Cep63 on tumor growth and proliferation . 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 and , indicating that Cep63 may be an important oncogene of PTC.
本研究旨在观察中心体蛋白 63(Cep63)在甲状腺乳头状癌(PTC)组织和细胞中的表达,并探讨 Cep63 在 PTC 中的表达临床意义。收集原发性 PTC 组织和配对的正常甲状腺组织,通过反转录-定量 PCR 和 Western blot 检测 Cep63 的表达水平。构建稳定的 Cep63 敲除细胞系,评估 Cep63 对细胞增殖、侵袭、迁移和凋亡能力的影响。建立裸鼠皮下肿瘤生成模型,评估 Cep63 对肿瘤生长和增殖的影响。Western blot 用于探讨相关信号通路。结果显示,PTC 组织中 Cep63 的表达水平明显升高。Cep63 敲除后 TPC-1 细胞的增殖、侵袭和迁移能力降低,沉默 Cep63 导致 TPC-1 细胞周期停滞在 S 期。机制上,Cep63 敲除抑制了 Janus 激酶/信号转导和转录激活因子 3 信号通路的激活。综上所述,Cep63 敲除显著抑制了 TPC-1 细胞的生物学功能,表明 Cep63 可能是 PTC 的一个重要癌基因。