KCNH2 regulates the growth and metastasis of pancreatic cancer

Abstract

Objective: Due to the characteristics of insidious onset and early metastasis of pancreatic cancer (PC), patients are often diagnosed at an advanced stage and often delayed in completing surgical resection timely, resulting in poor prognosis. Therefore, this study aims to explore the expression of potassium voltage-gated channel subfamily H member 2 (KCNH2) in PC and its relationship with clinicopathological parameters and the related mechanisms. Methods: GEPIA database and immunohistochemical staining were used to analyze the difference in KCNH2 expression between PC and adjacent tissue in RNA and protein levels. Chi-squared test was used to evaluate the relationship between KCNH2 expression and clinicopathological features. The Cox regression model was used for multivariate analysis and univariate analysis. Histological diagnosis was performed according to World Health Organization (WHO) criteria to evaluate the relationship between KCNH2 expression and clinicopathological features. Results: KCNH2 expression was upregulated in PC compared with normal pancreatic tissue. In addition, the knockdown of KCNH2 inhibits PC cell proliferation, migration, invasion, and epithelial-mesenchymal transformation and promotes their apoptosis. In addition, clinical data showed that the abnormal expression of KCNH2 in PC was related to the tumor stage. Patients with high expression of KCNH2 had a poor prognosis. Conclusions: KCNH2 is expected to be a novel targeted molecule in treating PC.