Interactions of Vascular Endothelial Growth Factor and p53 with miR-195 in Thyroid Carcinoma: Possible Therapeutic

Hamidreza Maroof1, Soussan Irani1,2, Armin Arianna1

  • 1Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland, Australia.

Abstract

Insights

MicroRNA-195 (miR-195) acts as a tumor suppressor in thyroid carcinoma by targeting VEGF-A and p53. Upregulating miR-195 inhibits cancer cell growth and induces apoptosis, suggesting therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Clinical and cellular mechanisms of miR-195 in thyroid carcinoma remain uninvestigated.
  • Thyroid carcinoma is a significant health concern with diverse clinical behaviors.

Purpose of the Study:

  • To elucidate the interactions between vascular endothelial growth factor (VEGF), p53, and miR-195 in thyroid carcinoma.
  • To investigate the clinical and pathological relevance of miR-195 in thyroid cancer.

Main Methods:

  • Real-time PCR to quantify miR-195 expression in 123 thyroid carcinomas, metastatic lymph nodes, and control tissues.
  • Western blot and immunofluorescence to assess the impact of exogenous miR-195 on VEGF-A and p53 protein levels.
  • Cell cycle and apoptosis assays to evaluate miR-195's role in cancer cell progression.

Main Results:

  • miR-195 expression was significantly downregulated in most papillary thyroid carcinoma tissues and cell lines.
  • Exogenous miR-195 introduction led to decreased VEGF-A and increased p53 protein expression.
  • Upregulation of miR-195 induced cell cycle arrest and apoptosis in thyroid carcinoma cells.

Conclusions:

  • miR-195 functions as a tumor suppressor in thyroid carcinoma, regulating cell cycle and apoptosis via VEGF-A and p53 targeting.
  • miR-195 represents a promising therapeutic target for aggressive thyroid carcinomas.

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