Elevated MRPS23 expression facilitates aggressive phenotypes in breast cancer cells.

Mitochondrial ribosomal protein S23 (MRPS23), encoded by a nuclear gene, is a well-known driver of proliferation in cancer. It participates in mitochondrial protein translation, and its expression association has been explored in many types of cancer. However, MRPS23 expression associations are rarely reported in breast cancer (BC). In this study, we explored the MRPS23 expression in BC cells compared with the non-tumoral breast cells. Overexpression and knockdown analysis of MRPS23 were performed in BC cells. Transfection efficiency was evaluated by western blot and qRT-PCR analysis. The role of MRPS23 in the malignant biological behaviors of BC cells was investigated using in-vitro experiments. Our results demonstrate that MRPS23 was aberrantly overexpressed at both the transcript and protein levels in BC cells. Additional findings reveal that deficiency of MRPS23 is associated with a decrease in cell proliferation/viability and compromised cell migration/invasion in BC cells. Relative to the sh-Ctrl group, the expression levels of cadherin, SNAI 1, and TWIST 1 decreased in the MRPS23 knockdown BC cells. We further found a significant decrease in the expression levels of Cyclin D1, Axin 2, LEF1, NKD1, and Survivin in MRPS23 knockdown cells. In conclusion, we found an association between MRPS23 knockdown and the metastasis ability of BC cells. These findings reveal that MRPS23 significantly decreases the migration and invasion of BC, thus inhibiting BC progression. We confirmed for the first time that MRPS23 expression determines the metastasis features of BC. Hence, the findings justify the key role of this protein in BC progression; therefore, it may be a potential therapeutic target for BC therapy.