Inhibitory effects of miR‑26b‑5p on thyroid cancer

Mol Med Rep. 2019 Aug;20(2):1196-1202. doi: 10.3892/mmr.2019.10315. Epub 2019 May 31.

Abstract

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.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Cell Proliferation*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Glycogen Synthase Kinase 3 beta / metabolism*
  • Humans
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • MicroRNAs / physiology
  • Middle Aged
  • Phosphorylation
  • Protein Processing, Post-Translational
  • Thyroid Neoplasms / genetics
  • Thyroid Neoplasms / metabolism*
  • Thyroid Neoplasms / physiopathology
  • Young Adult
  • beta Catenin / genetics*

Substances

  • CTNNB1 protein, human
  • MIRN526 microRNA, human
  • MicroRNAs
  • beta Catenin
  • Glycogen Synthase Kinase 3 beta