AI Article Synopsis
- Pancreatic cancer can be influenced by inflammation, particularly involving the NLRP3 inflammasome, which affects cancer cell growth and survival.
- The study tested how LPS-induced inflammation activates NLRP3 in pancreatic cancer cells and the effect of inhibiting it with MCC950 across different cell lines.
- Findings revealed that NLRP3 activation enhances cell proliferation by increasing caspase-1 and IL-1β production, while inhibiting NLRP3 with MCC950 reduced cell viability, with varying effectiveness depending on the specific cancer cell type.
Article Abstract
Purpose: Pancreatic cancer is a lethal form of cancer that can be triggered by prolonged or acute inflammation of the pancreas. Inflammation have been shown to be regulated by a group of key protein molecules known as the inflammasomes. The NLRP3 inflammasome is the most studied inflammasome and have been strongly implicated to regulate cancer cell proliferation. Therefore, this study aimed to examine the regulation of NLRP3 inflammasome under LPS-induced inflammation and its role in modulating cell proliferation in a panel of pancreatic cancer cells.
Methods: The effects of LPS-induced NLRP3 activation in the presence or absence of MCC950, NLRP3-specific inhibitor, was tested on a panel of three pancreatic cancer cell lines (SW1990, PANC1 and Panc10.05). Western blotting, cell viability kits and ELISA kits were used to examine the effects of LPS-induced NLRP3 activation and inhibition by MCC950 on NLRP3 expression, cell viability, caspase-1 activity and cytokine IL-1β, respectively.
Results: LPS-induced inflammation in the presence of ATP activates NLRP3 that subsequently increases pancreatic cancer cell proliferation by increasing caspase-1 activity leading to overall production of IL-1β. The inhibition of the NLRP3 inflammasome activation via the specific NLRP3 antagonist MCC950 was able to reduce the cell viability of pancreatic cancer cells. However, the efficacy of MCC950 varies between cell types which is most probably due to the difference in ASC expressions which have a different role in inflammasome activation.
Conclusion: There is a dynamic interaction between inflammasome that regulates inflammasome-mediated inflammation in pancreatic adenocarcinoma cells.
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| http://dx.doi.org/10.1007/s00432-020-03274-y | DOI Listing |
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