DPEP2 suppresses metastasis via NF-κB-mediated epithelial-mesenchymal transition and M2 polarization in p53-loss non-small cell lung cancer.

ABSTRACT: The TP53 gene (encoding the human p53 protein) is mutated in about 50% of non-small cell lung cancer (NSCLC). Loss of p53 is closely related to tumor metastasis and immune regulation, contributing to malignant progression and poor prognosis. However, therapeutic strategies for p53-loss NSCLC are still relatively limited. We found that DPEP2 is a diagnostic marker and predicts better outcome and prognosis in NSCLC with mutant TP53, but not with wild-type TP53. Loss of p53 induced DPEP2 downregulation at cellular and tissue levels. Functionally, DPEP2 inhibited the invasion and migration abilities, and decreased F-actin fibers. Mechanistically, DPEP2 impeded epithelial-mesenchymal transition (EMT) via the MAP3K7-mediated NF-κB signaling. Immunological analysis suggested that low level of DPE

SUBMITTER: Liu Y 

PROVIDER: S-EPMC12625370 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature