Knockdown of ectodysplasin‑A receptor‑associated adaptor protein exerts a tumor‑suppressive effect in tongue squamous cell carcinoma cells
- Meng Li
- Yu‑Ting Bai
- Kun Han
- Xiao‑Dong Li
- Jian Meng
Affiliations: Department of Stomatology, Central Hospital of Xuzhou, The Xuzhou Clinical College of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China
- Published online on: March 6, 2020 https://doi.org/10.3892/etm.2020.8578
Copyright: © Li
et al. This is an open access article distributed under the
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Tongue squamous cell carcinoma (TSCC) is a common malignancy in oral cancer with a high mortality and morbidity. The ectodysplasin‑A receptor‑associated adaptor protein (EDARADD) is a death domain‑containing adaptor protein that interacts with the TNF family ligand ectodysplasin A receptor. It is known that EDARADD has an effect on the development of ectodermal derivative tissues, such as hair and teeth. EDARADD expression is also associated with the development of melanoma. However, the role of EDARADD in TSCC remains unknown. The aim of the present investigation was to explore whether EDARADD plays a role in the biological function of TSCC. Immunohistochemistry was used to measure the expression of EDARADD in TSCC tissues and adjacent normal tissue. EDARADD was knocked down in a TSCC cell line in vitro using a specific lentivirus. The expression level of the EDARADD gene and the efficacy of gene knockdown were evaluated by reverse transcription‑quantitative PCR, while EDARADD protein expression and the expression levels of Bcl‑2, MYC and NF‑κBp65 were determined by western blotting. Additionally, MTT assays, colony formation assays and apoptosis assays were carried out to examine the effect of EDARADD knockdown on the TSCC cells. A previous study showed that the majority of the TSCC tissues that were tested had high EDARADD expression. The expression of EDARADD both at mRNA and protein levels was significantly lower (P<0.01) after the gene was knocked down in the CAL27 cells compared with the level in control cells. Downregulation of EDARADD expression inhibited colony formation and proliferation and induced apoptosis of CAL27 cells when compared to control cells (P<0.01). Taken together, these results suggested that EDARADD may be actively involved in the progression of TSCC and that EDARADD may be a novel therapeutic target for the treatment of TSCC.