PT  - JOURNAL ARTICLE
AU  - DEAN BALABANOV
AU  - LEI ZHAO
AU  - ZIWEN ZHU
AU  - ZACHARY E. HUNZEKER
AU  - HANNAH M. TONNER
AU  - VIVI A. DING
AU  - MARK R. WAKEFIELD
AU  - QIAN BAI
AU  - YUJIANG FANG
TI  - IL-29 Exhibits Anti-Tumor Effect on Pan-48 Pancreatic Cancer Cells by Up-regulation of P21 and Bax
AID  - 10.21873/anticanres.13495
DP  - 2019 Jul 01
TA  - Anticancer Research
PG  - 3493--3498
VI  - 39
IP  - 7
4099  - http://ar.iiarjournals.org/content/39/7/3493.short
4100  - http://ar.iiarjournals.org/content/39/7/3493.full
SO  - Anticancer Res2019 Jul 01; 39
AB  - Background/Aim: Pancreatic cancer is the most lethal cancer of the digestive system. IL-29 is a new member of the IFNλ family and well-known for its strong antiviral activity. However, its direct effect on pancreatic cancer is still unclear. This study was performed to investigate if IL-29 has any direct effect on Pan-48 pancreatic cancer cells. Materials and Methods: Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the effects of IL-29 on cell survival, proliferation, and apoptosis of Pan-48 pancreatic cancer cells. RT-PCR and IHC were subsequently performed to explore IL-29's potential molecular mechanisms. Results: The percentage of colonies of Pan-48 cells was decreased following the addition of IL-29. This was consistent with a decreased optical density (OD) value of cancer cells. Furthermore, the relative caspase-3 activity in cancer cells was increased after the addition of IL-29, indicating increased apoptosis of cancer cells. The anti-proliferative effect of IL-29 on cancer cells correlated with increased expression of the anti-proliferative molecule p21. The pro-apoptotic effect of IL-29 on cancer cells correlated with an increased expression of the pro-apoptotic molecule Bax. Conclusion: IL-29 constrains Pan-48 pancreatic cell growth via up-regulation of p21 and Bax. Our study suggests a potential use of IL-29 in immunotherapy for pancreatic cancer treatment.