Demethylation drug 5-Aza-2'-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro Retraction in /10.3892/ol.2021.12923

Jiang,Juan; Yi,Bo; Ding,Siqing; Sun,Jian; Cao,Wei; Liu,Mengzi

doi:10.3892/ol.2016.4364

Demethylation drug 5-Aza-2'-deoxycytidine-induced upregulation of miR-200c inhibits the migration, invasion and epithelial-mesenchymal transition of clear cell renal cell carcinoma in vitro

Retraction in: /10.3892/ol.2021.12923

Authors:
- Juan Jiang
- Bo Yi
- Siqing Ding
- Jian Sun
- Wei Cao
- Mengzi Liu
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Affiliations: Department of Nephrology, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of General Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China, Department of Nursing, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China
Published online on: March 22, 2016 https://doi.org/10.3892/ol.2016.4364
Pages: 3167-3172

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Abstract

The microRNA (miR)-200 family has been found to be involved in the process of mesenchymal-epithelial transition during renal development. Deregulation of miR-200c has been suggested to be involved in clear cell renal cell carcinoma (ccRCC). However, the precise role of miR‑200c in the regulation of ccRCC metastasis has not been previously reported. In the present study, it was observed that miR‑200c was frequently downregulated in ccRCC tissue compared with matched adjacent normal tissue. The expression of miR‑200c was additionally reduced in ccRCC cell lines when compared with levels in normal renal cells. The DNA demethylation drug 5‑Aza‑2'‑deoxycytidine (Aza) was used to treat several ccRCC cell lines, and it was observed that the expression of miR‑200c was significantly increased following Aza treatment. Furthermore, treatment with Aza markedly inhibited ccRCC cell invasion and migration, while treatment with miR‑200c inhibitor significantly enhanced invasion and migration of ccRCC cells. In addition, Aza treatment significantly promoted expression of E‑cadherin and inhibited the expression of N‑cadherin, while the inhibition of miR‑200c downregulated E‑cadherin and upregulated the expression of N‑cadherin, suggesting that miR‑200c has a suppressive role in epithelial-mesenchymal transition (EMT) of ccRCC cells. In conclusion, it was suggested that demethylation drug Aza-induced upregulation of miR‑200c may inhibit migration, invasion and EMT in ccRCC cells.

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