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J Cancer 2015; 6(8):767-775. doi:10.7150/jca.11833 This issue Cite

Research Paper

Deregulation of RGS17 Expression Promotes Breast Cancer Progression

Yuhua Li¹, Liliang Li¹, Junyi Lin¹, Xin Hu², Beixu Li¹, Aimin Xue¹, Yiwen Shen¹, Jieqing Jiang¹, Mingchang Zhang¹, Jianhui Xie^1✉, Ziqin Zhao^1✉

1. Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai, 200032, China.
2. Key Laboratory of Breast Cancer in Shanghai, Department of Breast Surgery, Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.

✉ Corresponding authors: Jianhui Xie, Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Email: jhxieedu.cn. Post Address: 138 Yixueyuan Road, Xuhui District, Shanghai, 200032, China. Telephone: 0086+021-54237569. Fax: 0086+021-64044561 or Ziqin Zhao, Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, Email: zqzhaoedu.cn. Post Address: 138 Yixueyuan Road, Xuhui District, Shanghai, 200032, China. Telephone: 0086+021-54237668. Fax: 0086+021-64044561 More

Abstract

Objective: A high level of RGS17 expression is observed in diverse human cancers and correlates with tumor progression. Herein, we aim to investigate its expression and function in breast cancer.

Methods: The expression of RGS17 was detected by immunohistochemical analysis and western blot analysis. The level of miR-32 expression was investigated by qRT-PCR. Western blot analysis was used to determine the relationship between RGS17 and miR-32. A series of loss or gain of function assays was performed to measure the effects of RGS17 or miR-32 on tumor migration, invasion, and proliferation.

Results: Compared to that in normal breast specimen, the expression of RGS17 had a significantly higher expression level in breast cancer tissues and cell lines. Although the potential relationship of RGS17 expression with clinicopathological features was not observed, there was a significant correlation of RGS17 expression with p63 expression. In cells, inhibition of RGS17 expression impaired cell migration, invasion, and proliferation. Further, RGS17 was identified as a direct and functional target of miR-32. Overexpression of miR-32 in cells could decrease the expression of RGS17 and inhibit cell migration, invasion, and proliferation. In contrast, ectopic expression of RGS17 could attenuate phenotypes caused by miR-32 overexpression.

Conclusion: The expression of RGS17 was upregulated in breast cancer, which could enhance cell migration, invasion, and proliferation. Moreover, the RGS17 was identified as a target of miR-32. Our results suggest that RGS17 might play an important role in breast cancer progression and could be a potential target for human breast cancer treatment.

Keywords: breast cancer, RGS17, p63, has-miR-32

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