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Updated: Feb 8, 2026

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
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.
Background:
The clinical pathological features, as well as the cellular mechanisms of miR-195, have not been investigated in thyroid carcinoma.
Objective:
The aim of this study is to identify the interactions of vascular endothelial growth factor (VEGF), p53 and miR-195 in thyroid carcinoma. The clinical and pathological features of miR-195 were also investigated.
Methods:
The expression levels of miR-195 were identified in 123 primary thyroid carcinomas, 40 lymph nodes with metastatic papillary thyroid carcinomas and seven non-neoplastic thyroid tissues (controls) as well as two thyroid carcinoma cell lines, B-CPAP (from metastasizing human papillary thyroid carcinoma) and MB-1 (from anaplastic thyroid carcinoma), by the real-time polymerase chain reaction. Using Western blot and immunofluorescence, the effects of exogenous miR-195 on VEGF-A and p53 protein expression levels were examined. Then, cell cycle and apoptosis assays were performed to evaluate the roles of miR-195 in cell cycle progression and apoptosis.
Results:
The expression of miR-195 was downregulated in majority of the papillary thyroid carcinoma tissue as well as in cells. Introduction of exogenous miR-195 resulted in downregulation of VEGF-A and upregulation of p53 protein expressions. Upregulation of miR-195 in thyroid carcinoma cells resulted in cell cycle arrest. Moreover, we demonstrated that miR-195 inhibits cell cycle progression by induction of apoptosis in the thyroid carcinoma cells.
Conclusion:
Our findings showed for the first time that miR-195 acts as a tumour suppressor and regulates cell cycle progression and apoptosis by targeting VEGF-A and p53 in thyroid carcinoma. The current study exhibited that miR-195 might represent a potential therapeutic target for patients with thyroid carcinomas having aggressive clinical behaviour.
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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