ArticleMedical oncology (Northwood, London, England)2025
RPL17 regulates the progression of breast cancer accompanied by MAPK signaling activation.
Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Breast cancer (BC) is the most frequently diagnosed cancer type and the leading cause of cancer-related mortality among females worldwide. This study aimed to investigate the role of RPL17 in BC. Our findings revealed that the expression of RPL17 in BC tissues and cell lines was significantly elevated compared to normal tissues and cells. The knockout of RPL17 in BC cell lines profoundly inhibited their proliferation, migration, invasion, and cell adhesion abilities. Furthermore, RPL17 knockout (RPL17-KO) cells exhibited increased apoptosis. Mechanistically, RPL17-KO cells demonstrated decreased MAPK signaling. Finally, the overexpression of RPL17 promoted the epithelial-mesenchymal transition (EMT) process in BC cells. RPL17-overexpressing cells displayed enhanced proliferation, migration, invasion, and cell adhesion abilities, alongside reduced apoptosis and increased MAPK signaling. Collectively, this study suggests that RPL17 functions as an important oncogene and may represent a potential therapeutic target for BC.
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