Evidence map›Paper›PMID 34211462›Full record

ArticleFrontiers in immunology2021

NLRP3 Inflammasome Promotes the Progression of Acute Myeloid Leukemia

Chaoqin Zhong, Ruiqing Wang, Mingqiang Hua, Chen Zhang, Fengjiao Han, Miao Xu, Xinyu Yang, Guosheng Li, Xiang Hu, Tao Sun and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  6. Pandora's Box of AML: HowBiomedicines · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Chaoqin ZhongDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Ruiqing WangDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Mingqiang HuaDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Chen ZhangDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Fengjiao HanDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Miao XuDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Xinyu YangDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Guosheng LiDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Xiang HuDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Tao SunDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Chunyan JiDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Daoxin MaDepartment of Hematology, Qilu Hospital of Shandong University, Jinan, China.
Qilu Hospital of Shandong University · CNYantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NLRP3 inflammasome has been reported to be associated with the pathogenesis of multiple solid tumors. However, the role of NLRP3 inflammasome in acute myeloid leukemia (AML) remains unclear. We showed that NLRP3 inflammasome is over-expressed and highly activated in AML bone marrow leukemia cells, which is correlated with poor prognosis. The activation of NLRP3 inflammasome in AML cells promotes leukemia cells proliferation, inhibits apoptosis and increases resistance to chemotherapy, while inactivation of NLRP3 by caspase-1 or NF-κB inhibitor shows leukemia-suppressing effects. Bayesian networks analysis and cell co-culture tests further suggest that NLRP3 inflammasome acts through IL-1β but not IL-18 in AML. Knocking down endogenous IL-1β or anti-IL-1β antibody inhibits leukemia cells whereas IL-1β cytokine enhances leukemia proliferation. In AML murine model, up-regulation of NLRP3 increases the leukemia burden in bone marrow, spleen and liver, and shortens the survival time; furthermore, knocking out NLRP3 inhibits leukemia progression. Collectively, all these evidences demonstrate that NLRP3 inflammasome promotes AML progression in an IL-1β dependent manner, and targeting NLRP3 inflammasome may provide a novel therapeutic option for AML.

Indexed as

AnimalsDisease Models, AnimalHumansInflammasomesInflammationInterleukin-1betaLeukemia, Myeloid, AcuteMacrophagesMiceNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 Proteinacute myeloid leukemiaIL-1βinflammasomeNLRP3progression

Identifiers

PMID34211462
PMCPMC8239362
OpenAlexW3118296868

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.