Abstract
The purpose of this study was to detect the expression of long non-coding ribonucleic acid 00163 (LINC00163) in human papillary thyroid cancer (PTC), and to observe the influence of downregulated LINC00163 on the proliferative and metastatic capacities of human PTC cells. Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) assay was applied to measure the expression level of LINC00163 in PTC tissues and para-carcinoma tissues, as well as that in normal human thyroid cells (Nthy-ori3-1) and PTC cells. After the expression of LINC00163 in PTC cells was interfered, qRT-PCR assay was performed to determine the interference efficiency, and colony formation and Cell Counting Kit-8 (CCK-8) assays were conducted to study the impacts of small interfering (si)-LINC00163 on the proliferative capacity of PTC cells. Moreover, wound healing and transwell assays were adopted to investigate the changes in the migratory and invasive abilities of PTC cells after the interference in the expression of LINC00163 in PTC cells. Finally, the changes in expressions of molecular markers in downstream signaling pathways after interference in LINC00163 expression were examined via Western blotting assay. In 51 cases of PTC tissues and corresponding para-carcinoma tissues, 41 cases exhibited an up-regulated expression of LINC00163, and qRT-PCR results indicated that PTC cells also had an up-regulated expression of LINC00163 compared with normal human thyroid cells. After the expression of LINC00163 in PTC cells was interfered, the results of colony formation and CCK-8 assays manifested that the proliferative capacity of the cells declined. It was also shown in wound-healing and transwell assay results that the migratory and invasive abilities of the cells were weakened. In addition, the results of Western blotting assay revealed expression changes in the molecular markers of epithelial-mesenchymal transition (EMT). The expression of LINC00163 in NSCLC tissues and cells is upregulated, and highly expressed LINC00163 can promote PTC cell proliferation and metastasis by regulating the EMT.
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