ARHI as a key regulator of EMT and metastasis in pancreatic cancer via the Notch-1 pathway.

Pancreatic cancer cell metastasis is a major factor influencing prognosis. A Ras homologue member I (ARHI) was reported to regulate proliferation and apoptosis in pancreatic cancer; however, its role in invasion remains unclear. This study aimed to explore the role and related mechanisms of ARHI in pancreatic cancer metastasis. We revealed that in pancreatic cancer ARHI expression levels were consistent with aggressive cellular phenotypes, and that changes in endogenous ARHI protein expression led to corresponding alterations in epithelial-mesenchymal transition (EMT) markers. Furthermore, ARHI accelerated tumor invasion in pancreatic cancer cells and in a mouse hepatic metastasis model. Notably, this unusual promoting effect of ARHI on EMT and invasion in pancreatic cancer was primarily exerted through the Notch-1 signaling pathway. Collectively, our findings provide insight into the function and molecular mechanisms of ARHI in pancreatic cancer metastasis.