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.