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Published on: August 23, 2019
TEAD4 overexpression suppresses thyroid cancer progression and metastasis in vitro by modulating Wnt signaling
Buyong Zhang1, Qingqing Wang, Yanting Ji
1Department of Thyroid and Breast, Cangzhou Central Hospital, Cangzhou, China.
Abstract:
TEAD4 has been reported to act as an oncogenic gene in various types of cancer. This study intends to investigate the role and regulatory mechanism of TEAD4 in thyroid cancer (TC). GEPIA was used to predict the expression pattern of TEAD4 in TC. Expressions of TEAD4 and wnt3a in TC tissues and cells were analyzed by qRT-PCR and Western blot. TC cells were transfected with TEAD4 overexpression plasmids and treated with or without IWR-1-endo (a Wnt signaling inhibitor), and then TC cell viability, migration and invasion were assessed by MTT and Transwell assay. Expressions of E-cadherin, N-cadherin and Vimentin in cells were analyzed by Western blot. TEAD4 was low-expressed in TC tissues and cells. TEAD4 overexpression inhibited the viability, inhibited migration and invasion of TC cells, and downregulated N-cadherin and Vimentin expression, while promoted E-cadherin and wnt3a expression. The wnt3a expression was positively correlated with TEAD4 expression in TC. IWR-1-endo treatment reversed the effect of TEAD4 in TC cells. TEAD4 overexpression suppresses TC progression and metastasis in vitro through modulating Wnt signaling.
Insights
Thyroid cancer (TC) progression is suppressed by TEAD4, a gene typically acting as oncogenic. TEAD4 overexpression inhibits tumor growth and metastasis by modulating Wnt signaling pathways.
Area of Science:
- Oncology
- Molecular Biology
Background:
- TEAD4 is implicated as an oncogene in multiple cancers.
- Its specific role and regulatory mechanisms in thyroid cancer (TC) require further elucidation.
Purpose of the Study:
- To investigate the function and regulatory mechanisms of TEAD4 in thyroid cancer.
- To determine if TEAD4 influences TC progression and metastasis.
Main Methods:
- Gene expression analysis (GEPIA, qRT-PCR, Western blot) of TEAD4 and wnt3a in TC tissues and cells.
- In vitro assays (MTT, Transwell) to assess TC cell viability, migration, and invasion following TEAD4 overexpression and Wnt signaling inhibition (IWR-1-endo).
- Analysis of epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Vimentin).
Main Results:
- TEAD4 was found to be downregulated in TC tissues and cells.
- Overexpression of TEAD4 suppressed TC cell viability, migration, and invasion.
- TEAD4 overexpression promoted E-cadherin and wnt3a expression while downregulating N-cadherin and Vimentin.
- TEAD4 expression positively correlated with wnt3a expression.
- Inhibition of Wnt signaling reversed the effects of TEAD4 overexpression.
Conclusions:
- TEAD4 acts as a tumor suppressor in thyroid cancer, contrary to its oncogenic role in other cancers.
- TEAD4 overexpression inhibits TC progression and metastasis in vitro.
- TEAD4 exerts its suppressive effects through the modulation of Wnt signaling.
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