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.
Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways