Papillary thyroid carcinoma (PTC) is the most prevalent cancer in the endocrine system, and the number of patients diagnosed with PTC has been increasing rapidly in recent years. Previous studies have reported that miR-145 plays an important role in many kinds of cancers, but its function in PTC remains unclear. In this study, we found that compared to paracancerous tissues, the level of miR-145 expression was significantly downregulated in PTC tissues.When miR-145 is overexpressed, migration and invasion of PTC cells were suppressed in vitro. In addition, we found that miR-145 downregulated the nuclear factor-κB (NF-κB) pathway in PTC cells. Taken together, our data suggest that miR-145 functions as a tumor suppressor in PTC with the suppressive effect related to downregulation of the NF-κB pathway. K E Y W O R D S invasion, migration, miR-145, NF-κB pathway, papillary thyroid carcinoma

In order to examine the inhibitory effects of microRNA (miR)-26b-5p on thyroid cancer (TC), the clinicopathological features and pathological tissues of 67 patients were collected. The expression levels of miR-26b-5p were detected in TC and paracarcinoma tissues by quantitative polymerase chain reaction, and the association between miR-26b-5p expression and the clinicopathological features of the patients was analyzed using t-test or one-way analysis of variance. In addition, B-CPAP TC cells were infected with a lentivirus to induce miR-26b-5p overexpression and proliferation was detected by Cell Counting kit-8. Subsequently, migration and invasion were detected by Transwell and Matrigel assays, respectively, and the molecular mechanism of action was investigated by western blotting. The results demonstrated that the expression levels of miR-26b-5p were significantly lower in TC tissues compared with paracarcinoma tissues (P<0.01), and miR-26b-5p was associated with lymph node metastasis (P<0.05). In addition, overexpression of miR-26b-5p inhibited the proliferation, invasion and migration of B-CPAP cells. Western blot analysis demonstrated that the protein expression levels of phosphorylated glycogen synthase kinase-3β (pGsk-3β) were decreased, and the expression of β-catenin was decreased in B-CPAP cells overexpressing miR-26b-5p. These results demonstrated that miR-26b-5p may exert antitumor activity. In addition, at the molecular level, these effects may be associated with the Gsk-3β/β-catenin pathway.

Papillary thyroid carcinoma (PTC) is the most common form of thyroid cancer, and its incidence is on the rise. It has been reported that some matrix metalloproteinases (MMPs) are abnormally expressed in PTC and can be used as diagnostic markers. However, few studies have explored the underlying mechanisms by which MMPs promote tumor progression. In this study, we used microarray analysis to compare the variations of gene expression within the PTC cell populations and their adjacent normal tissues and found that MMP-11 was the most differentially expressed MMP. To investigate the role of MMP-11 in the mediation of thyroid cancer cell development, pEnter-MMP-11 plasmid, and MMP-11 small interfering RNA were applied to up- and downregulate MMP-11 expression of in cultured PTC cell lines K1 and BCPAP. The results suggested that the levels of proliferation and migration of cells transfected with MMP-11 siRNA were significantly reduced, while the levels in MMP-11-plasmid-transfected cells were increased. In terms of the mechanism, experimental data showed that the change in cyclin D1 is consistent with MMP-11 expression, which may explain the changes in proliferation. In addition, Western blot assay was conducted to analyze the p65 and activated (phospho-) p65 protein levels concomitant with MMP-11 adjustments. Variations in intracellular MMP-11 significantly altered the amount of phospho-p65 in thyroid cells, while p65 knockdown did not affect MMP-11 expression. These results suggest that MMP-11 is located upstream of p65 and regulates its activity. Interestingly, the data for the Transwell assay suggested that MMP-11 regulatory migration is also associated with the NF-κB p65 signaling pathway. In conclusion, this report describes the important role of MMP-11 in the regulation of thyroid cell proliferation and migration. Mechanistic studies have shown that cyclin D1 and p65 are important mediators in the processes, which provides a new way to study the mechanism of MMPs promoting the progression of thyroid cancer.