KCNH2 Regulates the Growth and Metastasis of Pancreatic Cancer

Abstract

The mortality rate of pancreatic cancer (PC) remains high due to late diagnosis, early metastasis, and difficulty of complete resection. The online databases showed that potassium voltage-gated channel subfamily H member 2 (KCNH2) was highly expressed in pancreatic tumor tissues and was closely related to the poor survival of patients with PC. However, the mechanism of action of KCNH2 in PC is still unclear. In the present study, for the first time, we explored the regulatory effect of KCNH2 in PC. The results showed that KCNH2 was upregulated in PC compared with normal pancreatic tissues. High KCNH2 expression was associated with low tissue differentiation, high malignancy, and poor prognosis of PC. Moreover, knockdown of KCNH2 inhibited the proliferation and apoptosis of PC cells, as well as the epithelial-mesenchymal transition process, thereby promoting PC cell migration and invasion. In addition, KCNH2 knockdown inhibited the progression and metastasis of PC in a mouse xenograft model. In conclusion, these findings highlighted the potential of KCNH2 as a targeted molecule in the treatment of PC.