| Literature DB >> 30506430 |
Alicia A Manning1, Lei Zhao2, Ziwen Zhu3, Huaping Xiao1, Chase G Redington3, Vivi A Ding1, Theodore Stewart-Hester1, Qian Bai3, Jacob Dunlap3, Mark R Wakefield3, Yujiang Fang4,5,6.
Abstract
Pancreatic cancer is the most lethal digestive cancer and the fourth leading cause of cancer death in the US. IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer.Entities:
Keywords: Apoptosis; IL-39; Proliferation
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Year: 2018 PMID: 30506430 DOI: 10.1007/s12032-018-1236-y
Source DB: PubMed Journal: Med Oncol ISSN: 1357-0560 Impact factor: 3.064