POC1A induces epithelial–mesenchymal transition to promote growth and metastasis through the STAT3 signaling pathway in triple-negative breast cancer

作者：Yuzhou Qian, Yu Che, Shanqi Li, Xue Zhang, Qingshu Li, Yong Zhu, Long Wang, Xuedong Yin · 发表于：Molecular Medicine · 年份：2025 · DOI：10.1186/s10020-025-01315-1 · 被引用次数：3 · 研究领域：Microtubule and mitosis dynamics、Cancer Cells and Metastasis、Glycosylation and Glycoproteins Research

OBJECTIVES: Triple-negative breast cancer (TNBC) is known for its aggressiveness, which can be attributed to its heterogeneity, metastasis, and invasion capabilities. POC1 centriolar protein homolog A (POC1A), a centriolar protein involved in the formation of stable centrioles, has been associated with both cancer promotion and suppression in various malignant tumors. However, the underlying mechanisms that drive POC1A-induced metastases in TNBC remain to be elucidated. METHODS: The expression of POC1A changes and their clinical significance have been evaluated using TNBC tissues and a database. POC1A expression was examined in clinical samples and cells. The impacts of POC1A on the epithelial-mesenchymal transition's (EMT) relative factor expression was examined using immunofluorescence (IF), transcription-quantitative PCR (RT-qPCR), and Western blotting. We investigated the migration and invasion capabilities of TNBC cells and found that the patterns of tumor growth and metastasis varied correspondingly in different xenograft models. RNA sequencing (RNA-seq) was performed to explore the signaling pathways involved in POC1A, which was verified by several experiments. RESULTS: Our study identified an increase in the expression of POC1A in TNBC tissues, which was found to correlate with tumor size and lymph node metastasis. Meanwhile, POC1A plays a crucial role in the process of EMT, regulating the invasion and metastasis of TNBC in vitro and in vivo. Our RNA sequence results,...