Evidence map›Paper›PMID 32507974›Full record

ArticleJournal of cancer research and clinical oncology2020

The effects of NLRP3 inflammasome inhibition by MCC950 on LPS-induced pancreatic adenocarcinoma inflammation.

Alan Cheuk Keong Yaw, Elaine Wan Ling Chan, Jeremy Kean Yi Yap, Chun Wai Mai

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 40 citations in OpenAlex.

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  20. The role of NLRP3 inflammasome in digestive system malignancy.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Alan Cheuk Keong YawSchool of Postgraduate Studies, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Elaine Wan Ling ChanInstitute for Research, Development and Innovation, International Medical University, Jalan Jalil Perkasa 19, 126 Jalan 19/155B, Bukit Jalil, 57000, Kuala Lumpur, Malaysia. elainechan@imu.edu.my.ORCID http://orcid.org/0000-0002-8627-0161
Jeremy Kean Yi YapSchool of Postgraduate Studies, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Chun Wai MaiDepartment of Pharmaceutical Chemistry, School of Pharmacy, International Medical University, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
IMU University · MY

Funding

International medical university MMM 1-2019(02)
6 · The paper itself

Abstract

purposePancreatic 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.

methodsThe 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.

resultsLPS-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.

conclusionThere is a dynamic interaction between inflammasome that regulates inflammasome-mediated inflammation in pancreatic adenocarcinoma cells.

Indexed as

AdenocarcinomaCell Line, TumorCell SurvivalCytokinesFuransHeterocyclic Compounds, 4 or More RingsHumansIndenesInflammasomesInflammationInflammation MediatorsInterleukin-1betaLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinPancreatic NeoplasmsSulfonamidesCytokinesFuransHeterocyclic Compounds, 4 or More RingsIndenesInflammasomesInflammation MediatorsInterleukin-1betaLipopolysaccharidesN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanSulfonamidesSulfonesApoptosis-associated speck-like protein (ASC)LPS-induced inflammationMCC950NLPR3 inflammasome inhibitorNLRP3 inflammasomePancreatic cancer

Identifiers

PMID32507974
PMCPMC11804369
OpenAlexW3033464930

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.