Kunming Medical University, Yunnan 650500, China; Thyroid and Breast Surgery Department, The Second Affiliated Hospital of Kunming Medical University, Yunnan 650032, China.
The Yan'an Hospital of Kunming, China.
Cancer Genet. 2021 Aug;256-257:5-16. doi: 10.1016/j.cancergen.2021.02.008. Epub 2021 Mar 4.
Thyroid cancer is the most common malignancy in human endocrine system. Increasing evidence has indicated that p62 plays a key role in tumorigenesis. The roles and underlying molecular mechanisms of P62 in thyroid cancer, however, remain to be elucidated.
The expression levels of P62 in thyroid tumor tissues and thyroid cancer cells were detected by western blotting and qRT-PCR. Then, the effects of up-regulation or down-regulation of P62 on thyroid cancer cell proliferation, migration, invasion, cell cycle and apoptosis were measured by CCK-8 assay, transwell assay, flow cytometry and transwell assay, respectively. In terms of the mechanism, P62 could stimulate thyroid cancer progression by the activation of nuclear factor-kappa B (NF-κB) signaling pathway.
P62 was highly expressed in thyroid tumor tissues. Furthermore, high expression of p62 was observed in PTC cell lines, and especially in the K1 and TPC-1 cells. In vitro, the up-regulation of p62 promoted cell proliferation, migration, and invasion of thyroid cancer cells, whereas the knockdown of p62 resulted in the opposite effect. Knock-down of P62 increased the number of cells in the G0/G1 phase but reduced it in the S and G2/M phase. Moreover, we confirmed that overexpression of p62 inactivated NF-κB pathway with sequencing analysis and bioinformatics analysis.
This research work suggested that p62 could promote PTC cell proliferation, migration, and invasion via NF-κB signaling pathway. Furthermore, p62 is a potential biomarker which might be closely related to the tumorigenesis in PTC. Its potential role as a therapeutic target for PTC is worthy of further study.
甲状腺癌是人类内分泌系统最常见的恶性肿瘤。越来越多的证据表明 p62 在肿瘤发生中起关键作用。然而，P62 在甲状腺癌中的作用及其潜在的分子机制仍有待阐明。
通过 Western blot 和 qRT-PCR 检测甲状腺肿瘤组织和甲状腺癌细胞中 P62 的表达水平。然后，通过 CCK-8 测定、Transwell 测定、流式细胞术和 Transwell 测定分别测量上调或下调 P62 对甲状腺癌细胞增殖、迁移、侵袭、细胞周期和凋亡的影响。就机制而言，P62 可以通过激活核因子-κB（NF-κB）信号通路来刺激甲状腺癌的进展。
P62 在甲状腺肿瘤组织中高表达。此外，在 PTC 细胞系中观察到 p62 高表达，尤其是在 K1 和 TPC-1 细胞中。在体外，p62 的上调促进了甲状腺癌细胞的增殖、迁移和侵袭，而 p62 的下调则产生了相反的效果。p62 的敲低增加了 G0/G1 期的细胞数量，但减少了 S 和 G2/M 期的细胞数量。此外，我们通过测序分析和生物信息学分析证实，p62 的过表达使 NF-κB 通路失活。
这项研究工作表明，p62 可以通过 NF-κB 信号通路促进 PTC 细胞的增殖、迁移和侵袭。此外，p62 是一种潜在的生物标志物，可能与 PTC 的肿瘤发生密切相关。其作为 PTC 治疗靶点的潜在作用值得进一步研究。
