Abstract
Novel therapy strategies are crucial for thyroid carcinoma treatment. It is increasingly important to clarify the mechanism of thyroid carcinoma progression. Several studies demonstrate that α-Enolase (ENO1) participates in cancer development; nevertheless, the role of ENO1 in thyroid carcinoma progression remains unclear. In the present study, we found that the expression of ENO1 was upregulated in thyroid carcinoma samples. Proliferation and migration of thyroid carcinoma cells were suppressed by depletion of ENO1; conversely, ENO1 overexpression promoted thyroid carcinoma cell growth and invasion. To elucidate the mechanisms, we found that the hypoxia-related mTOR/HIF1 pathway regulated ENO1 expression. ENO1 regulated the expression of CST1; knockdown of CST1 reversed the tumorigenicity enhanced by ENO1 overexpression. Taken together, our findings provide a theoretical foundation for thyroid carcinoma treatment.
Highlights
The thyroid gland is the largest endocrine organ in humans; it regulates systemic metabolism (Kondo et al, 2006)
We found upregulation of ENO1 in thyroid carcinoma compared with normal samples (Figure 1A)
Tumor size enlargement was reduced to control levels with shCST1 treatment (Figures 8E–G). These findings suggest a synergistic role between ENO1 and CST1 in thyroid carcinoma progression. Traditional therapy strategies such as radioactive-iodine ablation and surgical resection are essential for thyroid carcinoma treatment
Summary
The thyroid gland is the largest endocrine organ in humans; it regulates systemic metabolism (Kondo et al, 2006). Thyroid carcinoma (THCA) is the most frequent malignancy in endocrine organs (Hundahl et al, 1998; Parkin et al, 2005; Kondo et al, 2006; Sipos and Mazzaferri, 2010). The increased incidence of thyroid carcinoma is most likely the result of a better understanding of the genetic pathogenesis and more efficient detection methods (Kondo et al, 2006; Sipos and Mazzaferri, 2010; La Vecchia et al, 2015; Davies, 2016).
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