Background
Pancreatic cancer (PC) is a highly aggressive malignancy with a poor prognosis due to its late-stage diagnosis and limited treatment options. Objectives: This study aimed to elucidate the molecular mechanisms underlying PC progression and identify potential molecular targets for its diagnosis and treatment.
Conclusions
DAZAP1 suppression promotes ferroptosis, thereby inhibiting PC cell proliferation and metastasis. These findings suggest that DAZAP1 is a potential therapeutic target for PC.
Methods
DAZAP1 expression in PC tissues, normal tissues and cell lines was assessed using immunohistochemistry (IHC), reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. DAZAP1 knockdown was achieved through plasmid transfection, and its effects on ferroptosis and PC progression were evaluated using RT-qPCR, western blotting, CCK-8 assays, EdU staining, Fe2+ content measurement, reactive oxygen species (ROS) detection, wound healing and Transwell migration assays.
Results
DAZAP1 expression was significantly upregulated in PC tissues and cell lines compared to normal counterparts. DAZAP1 knockdown suppressed PC cell proliferation and induced ferroptosis, while ferroptosis inhibition reversed these effects, enhancing PC cell proliferation and metastasis. Conclusions: DAZAP1 suppression promotes ferroptosis, thereby inhibiting PC cell proliferation and metastasis. These findings suggest that DAZAP1 is a potential therapeutic target for PC.