Down-regulation of MRPS23 inhibits rat breast cancer proliferation and metastasis
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Yan Gao1,*, Fuyan Li1,*, Hong Zhou1, Yi Yang1, Ruimin Wu1, Yijia Chen1, Wei Li1, Yang Li1, Xueqin Xu1, Changbin Ke1 and Zhijun Pei1
1 Department of PET Center and Institute of Anesthesiology and Pain, Taihe Hospital, Hubei University of medicine, Hubei, China
*These authors contributed equally to this work
Zhijun Pei, email: [email protected]
Changbin Ke, email: [email protected]
Keywords: MRPS23, breast cancer, metastasis, p53, p21 WAF1/CIP1
Received: October 31, 2016 Accepted: April 28, 2017 Published: May 15, 2017
Mitochondrial ribosomal protein S23 (MRPS23) has been shown to be involved in breast cancer cell proliferation and metastatic phenotypes of cervical cancer. Here we investigated its biological features in breast cancer for the first time. It demonstrated that knockdown of MRPS23 reduced breast cancer cell proliferation and induced apoptosis in vitro. Besides, shRNA targeting MRPS23 (shMRPS23) inhibited tumour proliferation and metastasis by blocking tumor angiogenesis in breast cancer xenograft rat model. Small animal positron emission tomography/computed tomography (PET/CT) with 2’-deoxy-2’-[18F] fluoro-D-glucose (FDG) was performed at four weeks after tumour cell injection. We found that FDG maximum standardized uptake value (SUVmax) significantly decreased by 31 ± 3% in the shMRPS23-treated group. But this change was not independent of metabolic tumour size. In addition, we also found that shMRPS23 could significantly suppress breast cancer metastasis through inhibiting epithelial mesenchymal transition (EMT) phenotype. The epithelial marker E-cadherin was increased, whereas the metastasis associated gene vimentin was decreased. Mechanistically, shMRPS23-treated tumours failed to progress through p53 and p21WAF1/CIP1 activation, but not cytochrome c-mediated pathway. These findings suggest that MRPS23 is a potential therapeutic target for interference of breast cancer proliferation, angiogenesis and metastasis.
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