MiR-204 regulates HMGA2 expression and inhibits cell proliferation in human thyroid cancer

Cancer Biomark. 2015;15(5):535-42. doi: 10.3233/CBM-150492.

Abstract

Background: Analysis using publicly available algorithms has found that high mobility group AT-hook 2 (HMGA2), a key transcriptional regulatory factor, is a potential target of microRNA-204 (miR-204). Some studies have shown that both miR-204 and HMGA2 are associated with cancer development.

Objective: We examined the possible relationship between miR-204 and HMGA2 in the development of thyroid cancer.

Methods: We assessed miR-204 expression in thyroid cancer specimens and cell lines using real-time polymerase chain reaction (PCR). Luciferase reporter assay was used to confirm the target associations. The effect of miR-204 on cell proliferation was confirmed with tetrazolium and colony formation assays. Gene and protein expression were examined using real-time PCR and western blotting, respectively.

Results: MiR-204 was downregulated in the thyroid cancer specimens and cell lines, and targeted the 3^\prime untranslated region of HMGA2 directly. MiR-204 overexpression decreased cyclin D1 and Ki67 expression and increased P21 expression, which subsequently inhibited thyroid cancer cell proliferation.

Conclusions: Our findings suggest that miR-204 plays a protective role by inhibiting thyroid cancer cell proliferation, and may identify new targets for anti-cancer treatment.

Keywords: HMGA2; MiR-204; proliferation; thyroid cancer.

MeSH terms

  • Biomarkers, Tumor / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Gene Expression Regulation, Neoplastic
  • HMGA2 Protein / biosynthesis*
  • HMGA2 Protein / genetics
  • Humans
  • MicroRNAs / biosynthesis
  • MicroRNAs / genetics*
  • Thyroid Neoplasms / genetics*
  • Thyroid Neoplasms / pathology

Substances

  • Biomarkers, Tumor
  • HMGA2 Protein
  • MIRN204 microRNA, human
  • MicroRNAs