Background

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.

Methods

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.

Results

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.

Conclusion

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.

中文翻译：

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P62在人甲状腺癌发生发展中的作用及其可能机制

 背景

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在肿瘤发生中发挥着关键作用。然而，P62 在甲状腺癌中的作用和潜在分子机制仍有待阐明。

 方法

采用western blotting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。然后分别通过CCK-8实验、Transwell实验、流式细胞仪和Transwell实验检测P62上调或下调对甲状腺癌细胞增殖、迁移、侵袭、细胞周期和凋亡的影响。从机制上看，P62可以通过激活核因子-κB（NF-κB）信号通路来刺激甲状腺癌进展。

 结果

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的上调促进甲状腺癌细胞的增殖、迁移和侵袭，而p62的敲低则产生相反的效果。 P62 的敲除增加了 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的过度表达使NF-κB通路失活。

 结论

该研究工作表明p62可以通过NF-κB信号通路促进PTC细胞增殖、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。