The CPT1A/Snail axis promotes pancreatic adenocarcinoma progression and metastasis by activating the glycolytic pathway

Recent studies have demonstrated that CPT1A plays a critical role in tumor metabolism and progression. However, the molecular mechanisms by which CPT1A affects tumorigenicity during PAAD progression remain unclear. In the current research, the bioinformatics analysis and immunohistochemical staining results showed that CPT1A was overexpressed in PAAD tissues and that its overexpression was associated with a shorter survival time in patients with PAAD. Overexpression of CPT1A increased cell proliferation and promoted EMT and glycolytic metabolism in PAAD cells. Mechanistically, CPT1A is able to bind to Snail and facilitate PAAD progression by regulating Snail stability. In summary, our findings revealed Snail-dependent glycolysis as a crucial metabolic pathway by which CPT1A accelerates PAAD progression. Targeting the CPT1A/Snail/glycolysis axis in PAAD to suppress cell proliferation and metastatic dissemination is a new potential treatment strategy to improve the anticancer therapeutic effect and prolong patient survival.

Automated summary

Recent studies have shown that CPT1A plays a critical role in the metabolism and progression of pancreatic ductal adenocarcinoma (PAAD). Overexpression of CPT1A promotes cell proliferation and glycolytic metabolism in PAAD cells. Mechanistically, CPT1A binds to Snail and regulates its stability, thereby facilitating PAAD progression.