The role of P62 in the development of human thyroid cancer and its possible mechanism
| Autor: | Shou-Jun Deng, Ying Mao, Jun-Feng Ma, Ruo-Chuan Cheng, Ying Peng, Yanjun Su, Chang Diao |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
endocrine system diseases Apoptosis Protein Serine-Threonine Kinases Biology medicine.disease_cause 03 medical and health sciences 0302 clinical medicine Cell Movement Cell Line Tumor Sequestosome-1 Protein Genetics medicine Humans Neoplasm Invasiveness RNA Messenger Thyroid Neoplasms Molecular Biology Thyroid cancer Cell Proliferation Cell growth Cell Cycle Thyroid NF-kappa B Cancer Cell cycle medicine.disease Up-Regulation Gene Expression Regulation Neoplastic medicine.anatomical_structure 030220 oncology & carcinogenesis Disease Progression Cancer research Signal transduction Carcinogenesis Signal Transduction |
| Zdroj: | Cancer Genetics. :5-16 |
| ISSN: | 2210-7762 |
| DOI: | 10.1016/j.cancergen.2021.02.008 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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