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

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, followed by further investigation, revealed that POC1A promotes the metastasis of TNBC by inducing EMT through the STAT3 signaling pathway.

Conclusions: In short, for the first time, we have identified that POC1A plays a pivotal role in regulating the EMT of TNBC.