Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 118, Issue 12, Pages 4745-4752Publisher
WILEY
DOI: 10.1002/jcb.26142
Keywords
PTC; PTCSC3; miR-574-5p; Wnt/beta-CATENIN; PROLIFERATION; MIGRATION
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The distance metastases of papillary thyroid carcinoma (PTC) were a major threaten for PTC patients, thus, to study the potential mechanism for the treatment of PTC was essential. Previous studies have shown that PTCSC3 (Thyroid Carcinoma Susceptibility Candidate 3), miR-574-5p and Wnt/-catenin were involved in PTC, but the potential pathogenic mechanism among them was still unclear. Real-time PCR and Western blot were used to detect genes expression. Luciferase reporter assay was used to detect the combination of miR-574-5p and suppressor of cancer cell invasion (SCAI), as well as the ratio of TOP/FOP. RNA Pull-down assay verified the bound of PTCSC3 and miR-574-5p. MTT assay, Transwell assay, and wound scratch assay were used to detect cell viability and cell migration. The expression of PTCSC3 and SCAI were decreased, while miR-574-5p and -catenin were increased in PTC tissues and cells. Overexpressed PTCSC3 suppressed cell proliferation and migration, promoted the expression of SCAI, but inhibited -catenin. PTCSC3 absorbed miR-574-5p, and miR-574-5p targeted to SCAI; SCAI could regulate the activity of Wnt/-catenin. PTCSC3/miR-574-5p regulated the activity of Wnt/-catenin via SCAI and mediated cell proliferation and migration of PTC-1. In vivo experiments verified the fact that overexpressed PTCSC3 inhibited tumor growth. The signaling PTCSC3-miR-574-5p-SCAI-Wnt/-catenin mediated the proliferation and migration of PTC-1 cells, which was vital for the further PTC therapy and prognosis. J. Cell. Biochem. 118: 4745-4752, 2017. (c) 2017 Wiley Periodicals, Inc.
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