ArticleCancer gene therapy2026
PAK4 orchestrates dual transcriptional and post-translational repression of E-cadherin to promote epithelial-to-mesenchymal transition and invasiveness in pancreatic cancer.
Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a poor prognosis and a high propensity for metastasis. Analysis of TCGA data revealed that PAK4 overexpression was associated with inferior survival outcomes in PDAC patients. In this preclinical study, PAK4-amplified PDAC cells significantly enhanced migratory capacity compared to wild-type cells. Knockdown of PAK4 in these cells suppressed migration by increasing and stabilizing E-cadherin, accompanied by decreased Cdc42 activity. Conversely, constitutive expression of Flag-PAK4 in wild-type cells reduced E-cadherin levels while promoting cell migration, invasion, and motility through elevated Cdc42 activity. Immunoprecipitation and immunofluorescence analysis confirmed that PAK4 physically interacted with E-cadherin and Cdc42, with evident colocalization of these proteins. In an orthotopic PDAC mouse model, PAK4 knockdown reduced primary tumor burden and prevented malignant ascites, mediated by E-cadherin activation and stabilization. Notably, an inverse correlation between PAK4 and E-cadherin expression was also observed in pancreatic cancer patients' specimens. Collectively, these findings suggest that PAK4 drives invasive and metastatic phenotypes in PDAC by modulating E-cadherin and that targeting PAK4 may represent a promising therapeutic strategy for PDAC treatment.
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