BTG1 potentiates apoptosis and suppresses proliferation in renal cell carcinoma by interacting with PRMT1

Liu,Chunhui; Tao,Tao; Xu,Bin; Lu,Kai; Zhang,Lei; Jiang,Liang; Chen,Shuqiu; Liu,Dachuang; Zhang,Xiaowen; Cao,Nihao; Chen,Ming

doi:10.3892/ol.2015.3293

August-2015 Volume 10 Issue 2

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August-2015 Volume 10 Issue 2

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Article Open Access

BTG1 potentiates apoptosis and suppresses proliferation in renal cell carcinoma by interacting with PRMT1

Authors:
- Chunhui Liu
- Tao Tao
- Bin Xu
- Kai Lu
- Lei Zhang
- Liang Jiang
- Shuqiu Chen
- Dachuang Liu
- Xiaowen Zhang
- Nihao Cao
- Ming Chen
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Affiliations: Department of Urology, Affiliated Zhongda Hospital of Southeast University, Nanjing, Jiangsu 210009, P.R. China, Department of Urology, Haimen City People's Hospital, Haimen, Jiangsu 226100, P.R. China

Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 619-624
|
Published online on: May 29, 2015

https://doi.org/10.3892/ol.2015.3293
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Abstract

B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of Erb family. BTG1 regulates cell cycle progression, inhibits proliferation, promotes apoptosis and stimulates cellular differentiation in multiple cell types. However, the functions of BTG1 in renal cell carcinoma (RCC) remain unclear. Therefore, the present study investigated the role of BTG1 in RCC tissue samples and 786‑O RCC cells. RCC tissues and cells exhibited significantly weaker BTG1 protein and mRNA expression compared with para‑carcinoma control tissues (P<0.05). Upregulated BTG1 expression induced significant G0/G1 cell cycle arrest, apoptosis and inhibition of cell proliferation in 786‑O cells (P<0.05). Furthermore, BTG1 interacted with protein arginine N‑methyltransferase 1 (PRMT1), and blocking the action of PRMT1 in 786‑O cells resulted in inhibition of BTG1 function. These findings indicate that BTG1 may inhibit cell growth and promote apoptosis by interacting with PRMT1 in RCC; the identification of this mechanism may aid in the production of novel therapies for RCC.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

BTG1 potentiates apoptosis and suppresses proliferation in renal cell carcinoma by interacting with PRMT1

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