KCNN4-mediated Ca²⁺/MET/AKT axis is promising for targeted therapy of pancreatic ductal adenocarcinoma.

ABSTRACT: As a member of the potassium calcium-activated channel subfamily, increasing evidence suggests that KCNN4 was associated with malignancies. However, the roles and regulatory mechanisms of KCNN4 in PDAC have been little explored. In this work, we demonstrated that the level of KCNN4 in PDAC was abnormally elevated, and the overexpression of KCNN4 was induced by transcription factor AP-1. KCNN4 was closely correlated with unfavorable clinicopathologic characteristics and poor survival. Functionally, we found that overexpression of KCNN4 promoted PDAC cell proliferation, migration and invasion. Conversely, the knockdown of KCNN4 attenuated the growth and motility of PDAC cells. In addition to these, knockdown of KCNN4 promoted PDAC cell apoptosis and led to cell cycle arrest in the S phase. I

SUBMITTER: Mo X 

PROVIDER: S-EPMC8888650 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature