Abstract
BackgroundThyroid cancer is the most common type of endocrine malignancy and the incidence rate is rapidly increasing worldwide. Epigallocatechin-3-gallate (EGCG) could suppress cancer growth and induce apoptosis in many types of cancer cells. However, the mechanism of action of EGCG on the growth of human thyroid carcinoma cells has not been fully illuminated.MethodsCell proliferation and viability were detected by EdU and MTS assays. Cell cycle distribution was measured by flow cytometry. Migration and invasion were evaluated by scratch and transwell assays. Apoptotic levels were detected by TUNEL staining and western blotting. The protein levels of EGFR/RAS/RAF/MEK/ERK signaling pathway were detected by western blotting. The in vivo results were determined by tumor xenografts in nude mice. The in vivo proliferation, tumor microvessel density, and apoptosis were detected by immunohistochemistry.ResultsEGCG inhibited the proliferation, viability, and cell cycle progression in human thyroid carcinoma cells. EGCG decreased the migration and invasion, but increased the apoptosis of human thyroid carcinoma cells. EGCG reduced the protein levels of phospho (p)-epidermal growth factor receptor (EGFR), H-RAS, p-RAF, p-MEK1/2, and p-extracellular signal-regulated protein kinase 1/2 (ERK1/2) in human thyroid carcinoma cells. EGCG inhibited the growth of human thyroid carcinoma xenografts by inducing apoptosis and down-regulating angiogenesis.ConclusionsEGCG could reduce the growth and increase the apoptosis of human thyroid carcinoma cells through suppressing the EGFR/RAS/RAF/MEK/ERK signaling pathway. EGCG can be developed as an effective therapeutic agent for the treatment of thyroid cancer.
Highlights
Thyroid cancer is the most common type of endocrine malignancy and the incidence rate is rapidly increasing worldwide
EGCG inhibits the proliferation, viability, and cell cycle progression in human thyroid carcinoma cells As shown in Fig. 1, the proliferation and viability of TT, TPC-1, and ARO cells were inhibited by 10–200 μM EGCG in a dose-dependent manner
Our results showed that 10–200 μM EGCG increased the proportion of cells entering the S phase and decreased the proportion of cells entering the G2 phase (Fig. 2), indicating that EGCG could induce cell cycle arrest at S phase in human thyroid carcinoma cells
Summary
Thyroid cancer is the most common type of endocrine malignancy and the incidence rate is rapidly increasing worldwide. The mechanism of action of EGCG on the growth of human thyroid carcinoma cells has not been fully illuminated. Thyroid cancer is the most common endocrine malignancy with increasing incidence in recent years [1, 2]. Thyroid cancer of follicular cell origin accounts for the majority of thyroid malignancies, with other cancers deriving from parafollicular cells, namely medullary thyroid cancer (MTC) [3]. Follicular cell-derived cancers include differentiated follicular thyroid cancer (FTC) and papillary thyroid cancer (PTC), as well as the undifferentiated anaplastic thyroid cancer (ATC). FTC and PTC can further progress to poorly differentiated thyroid cancer [5,6,7]. It is an urgent need to develop novel agents/drugs for the treatment of thyroid carcinoma
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