Notch signaling molecule is involved in the invasion of MiaPaCa2 cells induced by CoCl(2) via regulating epithelial-mesenchymal transition

Pancreatic cancer exhibits a high mortality rate resulting from metastasis and there is currently no effective treatment strategy. Hypoxia serves an important role in cancer cells, where cellular metabolic rate is high. The underlying mechanisms that trigger hypoxia and the invasion of pancreatic cancer cells remain unknown. Investigation of the importance of hypoxia in the invasion of pancreatic cancer cells for potential, novel treatment strategies is of primary concern. Cell Counting Kit-8 assay, invasion assay, western blotting and reverse transcription-quantitative polymerase chain reaction were used to investigate invasion and epithelial mesenchymal transition (EMT) and the expression of Notch1 in MiaPaCa2 cells treated with cobalt II chloride (CoCl(2)). Hypoxia-inducible factor 1α (HIF-1α) small interfering (si)RNA and Notch1 inhibitor N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) were also selected to investigate these mechanisms. Data indicated that CoCl(2) increased the invasion ability and altered EMT in MiaPaCa2 cells. CoCl(2) regulated the expression of HIF-1α and Notch1 in MiaPaCa2 cells. In addition, HIF-1α siRNA inhibited the effects of CoCl(2) on the expression of Notch1 and decreased Snail, EMT and invasion in MiaPaCa2 cells. DAPT increased the expression of epithelial-cadherin and decreased the content of neural-cadherin, Snail and invasion in MiaPaCa2 cells in the presence or absence of CoCl(2). CoCl(2) promoted invasion by stimulating the expression of HIF-1α and regulating the expression of Notch1 and EMT in MiaPaCa2 cells. Targeting the Notch1 signaling molecule may be a novel treatment strategy for the prevention and treatment of pancreatic cancer.