Inhibin β-A (INHBA) induces epithelial-mesenchymal transition and accelerates the motility of breast cancer cells by activating the TGF-β signaling pathway.

Accumulating evidence indicates that INHBA (Inhibin β-A, a member of the TGF-β superfamily) functions as an oncogene in cancer progression. However, little is known as to how INHBA regulates the progression and aggressiveness of breast cancer (BC). This study explored the function and underlying mechanism of INHBA in epithelial-mesenchymal transition (EMT) of BC cells. INHBA expression in BC cell lines was measured using RT-qPCR and Western blot. The would-healing and transwell migration assays were used to investigate the effect of INHBA overexpression or silencing on BC cell motility. Moreover, the expression levels of EMT-related genes were quantified after overexpressing or silencing of INHBA. Based on published dataset, INHBA was significantly upregulated in BC tissues compared to the adjacent normal tissues. A higher level of INHBA expression was also correlated with a poor survival in BC patients. In addition, in vitro study showed that INHBA played an indispensable role in promoting BC cell proliferation and invasion. Mechanistically, INHBA induced epithelial-mesenchymal transition (EMT) and accelerated the motility of BC cells by activating TGF-β-regulated genes. In conclusion, INHBA plays a functional role in supporting EMT phenotype of BC cells, and it may serve as a diagnostic biomarker and a potential therapeutic target for BC treatment.