Department of Head and Neck Surgery, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan, China.
Department of Gynecology, Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Bioengineered. 2021 Dec;12(1):1299-1310. doi: 10.1080/21655979.2021.1911533.
Differentiated thyroid carcinoma (DTC) is one of the most common malignant tumors. Increasing evidence indicates that centromere protein K(CENPK) may play a key role in promoting carcinogenesis. The expression, biological functions, and clinical significance of CENPK in DTC are still unclear. The CENPK expression in the DTC specimen was confirmed using quantitative real-time PCR and Western blot. The expression of CENPK was silenced and promoted by lentivirus-mediated transfection with shRNA sequences or CENPK plasmid targeting CENPK in TPC1 and FTC-133 cells, respectively. Colony formation, Cell Counting Kit-8 (CCK-8), Transwell invasion, and scratch assays were performed to assess the malignant biological properties of FTC-133 and TPC1 cells. Tumorigenicity assay was performed using C57BL/6 mice to explore the influence of CENPK on the growth of TPC1. The present work suggested that the expression of CENPK remarkably increased in follicular thyroid cancer and papillary thyroid cancer tissue samples at the mRNA level. Immunohistochemical staining also showed consistent results at the protein level. In addition, CENPK mRNA expression level showed great value in diagnosis of DTC. Knockdown of CENPK significantly inhibited the invasion and migration of TPC1 and FTC-133 cells. In contrast, CENPK overexpression promoted invasion and migration of TPC1 and FTC-133 cells. Knockdown and overexpression of CENPK showed consistent effect on DTC tumor growth and expression of Ki-67 invivo. Our results indicated that CENPK was evidently upregulated in DTC. Knocking down CENPK suppressed TPC1 cell proliferation, invasion and migration. Targeting the CENPK may be anovel therapeutic method for DTC.
甲状腺分化癌（DTC）是最常见的恶性肿瘤之一。越来越多的证据表明着丝粒蛋白 K（CENPK）可能在促进癌变中发挥关键作用。CENPK 在 DTC 中的表达、生物学功能和临床意义尚不清楚。通过定量实时 PCR 和 Western blot 验证了 DTC 标本中的 CENPK 表达。通过慢病毒介导的 shRNA 序列或针对 CENPK 的 CENPK 质粒转染，分别沉默和促进 TPC1 和 FTC-133 细胞中的 CENPK 表达。通过集落形成、细胞计数试剂盒-8（CCK-8）、Transwell 侵袭和划痕实验评估 FTC-133 和 TPC1 细胞的恶性生物学特性。使用 C57BL/6 小鼠进行肿瘤发生测定，以研究 CENPK 对 TPC1 生长的影响。本工作表明，CENPK 在滤泡性甲状腺癌和乳头状甲状腺癌组织样本中的 mRNA 水平显著增加。免疫组织化学染色在蛋白质水平也显示出一致的结果。此外，CENPK mRNA 表达水平在 DTC 诊断中具有重要价值。敲低 CENPK 显著抑制了 TPC1 和 FTC-133 细胞的侵袭和迁移。相反，CENPK 过表达促进了 TPC1 和 FTC-133 细胞的侵袭和迁移。CENPK 的敲低和过表达对体内 DTC 肿瘤生长和 Ki-67 的表达具有一致的影响。我们的结果表明，CENPK 在 DTC 中明显上调。敲低 CENPK 抑制了 TPC1 细胞的增殖、侵袭和迁移。靶向 CENPK 可能是治疗 DTC 的一种新方法。
