MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1 Retraction in /10.3892/etm.2021.10628

Zou,Quanqing; Tang,Qianli; Pan,Yinhua; Wang,Xuedi; Dong,Xiaofeng; Liang,Zhongxiao; Huang,Dong

doi:10.3892/etm.2017.4590

MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1

Retraction in: /10.3892/etm.2021.10628

Authors:
- Quanqing Zou
- Qianli Tang
- Yinhua Pan
- Xuedi Wang
- Xiaofeng Dong
- Zhongxiao Liang
- Dong Huang
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Affiliations: Department of Breast Surgery, First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China, Department of General Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, P.R. China, Department of Hepatobiliary and Endocrine Surgery, People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, P.R. China
Published online on: June 13, 2017 https://doi.org/10.3892/etm.2017.4590
Pages: 1009-1016
Copyright: © Zou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNAs (miRs), which are a class of small non-coding RNAs, are key regulators of gene expression via induction of translational repression or mRNA degradation. However, the molecular mechanism of miR‑22 underlying the malignant progression of breast cancer, remains to be elucidated. The present study aimed to explore the regulatory mechanism of miR‑22 in breast cancer cell growth and metastasis. Reverse transcription‑quantitative polymerase chain reaction data revealed that miR‑22 was significantly downregulated in breast cancer tissues, compared with adjacent non‑tumor tissues. Furthermore, the miR‑22 levels were further decreased in stage III‑IV, compared with stage I‑II breast cancer. In addition, low miR‑22 levels were significantly associated with the poor differentiation, metastasis and advanced clinical stages of breast cancer. Sirtuin1 (SIRT1) was demonstrated to act as a direct target gene of miR‑22 and its protein expression negatively regulated by miR‑22 in the MCF‑7 breast cancer cell line. Furthermore, SIRT1 expression levels were significantly upregulated in breast cancer tissues, compared with adjacent non‑tumor tissues. SIRT1 levels were observed to be increased in stage III‑IV when compared with stage I‑II breast cancer. miR‑22 overexpression decreased the proliferation, migration and invasion of MCF‑7 cells, whereas overexpression of SIRT1 eliminated the suppressive effects of the miR‑22 overexpression on the malignant phenotype of MCF‑7 cells. The results of the present study therefore suggested that miR‑22 demonstrated suppressive effects on breast cancer growth and metastasis via targeting SIRT1, and thus the miR‑22/SIRT1 axis may be used as a novel and potential therapeutic target for breast cancer in the future.

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