Journal
ONCOLOGY LETTERS
Volume 21, Issue 6, Pages -Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2021.12699
Keywords
tumor necrosis factor-related apoptosis-inducing ligand (TRAIL); TRAIL-Mu3; death receptor; apoptosis; pancreatic cancer
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Funding
- National Natural Scientific Foundation of China [81372444]
- Natural Science Foundation of Chengdu Medical College [CYZ18-15]
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TRAIL-Mu3 exhibits stronger antitumor effects on pancreatic cancer cells compared with TRAIL by enhancing the apoptotic signaling pathway.
Pancreatic cancer is a highly malignant type of cancer and its treatment remains a major challenge. The novel recombinant protein TNF-related apoptosis-inducing ligand (TRAIL)-Mu3 has been shown to exert stronger tumor inhibitory effects in colon cancer in vitro and in vivo compared with TRAIL. The present study investigated the antitumor effects of TRAIL-Mu3 on pancreatic cancer cells, and the possible mechanisms were further examined. Compared with TRAIL, TRAIL-Mu3 exhibited significantly higher cytotoxic effects on pancreatic cancer cell lines. The inhibitory effect of TRAIL-Mu3 on the viability of PANC-1 cells was shown to be a caspase-dependent process. The affinity of TRAIL-Mu3 to PANC-1 cell membranes was significantly enhanced compared with TRAIL. In addition, TRAIL-Mu3 upregulated death receptor (DR) expression in PANC-1 cells and promoted the redistribution of DR5 in lipid rafts. Western blotting results demonstrated that TRAIL-Mu3 activated the caspase cascade in a faster and more efficient manner compared with TRAIL in PANC-1 cells. Therefore, TRAIL-Mu3 enhanced the antitumor effects in pancreatic cancer cells by strengthening the apoptotic signaling pathway. The present study indicated the potential of TRAIL-Mu3 for the treatment of pancreatic cancer.
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