Evidence map›Paper›PMID 32165863›Full record

ArticleCancer cell international2020

Sirtuin 1 inhibits lipopolysaccharide-induced inflammation in chronic myelogenous leukemia k562 cells through interacting with the Toll-like receptor 4-nuclear factor κ B-reactive oxygen species signaling axis.

Lei Wang, Mingming Wang, Hongju Dou, Wenjie Lin, Lifang Zou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Lei WangDepartment of Hematology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 639, Manufacturing Bureau Road, Shanghai, 200011 China.
Mingming WangDepartment of Hematology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 639, Manufacturing Bureau Road, Shanghai, 200011 China.
Hongju DouDepartment of Hematology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 639, Manufacturing Bureau Road, Shanghai, 200011 China.
Wenjie LinDepartment of Hematology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 639, Manufacturing Bureau Road, Shanghai, 200011 China.
Lifang ZouDepartment of Hematology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, No. 639, Manufacturing Bureau Road, Shanghai, 200011 China.ORCID 0000-0002-5998-1793
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic myelogenous leukemia (CML) is a clonal myeloproliferative neoplasm resulting from BCR-ABL-transformed hematopoietic stem cells. Previous research has implicated multifunctional proinflammatory cytokines in CML development. It has been reported that Sirtuin 1 (SIRT1) as well as ADP-ribosyltransferase and deacetylase may influence CML cell viability and inflammation.

methodsThis study was directed toward exploring the SIRT1-involved in the mechanism of lipopolysaccharide (LPS)-triggered inflammation in CML k562 cells.

resultsIn our study, the LPS-induced inflammation in k562 cells was reflected by increases in levels of diverse inflammatory cytokines, including interleukin (IL)-10, IL-1β, IL-6, interferon-γ, tumor necrosis factor (TNF)-α and TNF-β. LPS also decreased SIRT1 expression and nuclear location in k562 cells. Furthermore, SIRT1 overexpression inhibited the release of the above mentioned cytokines in LPS-treated cells. We also determined that LPS stimulation could activate Toll-like receptor 4 (TLR4), the nuclear factor κ B (NFκB) subunit, and p65 and produce reactive oxygen species (ROS) in k562 cells. Nevertheless, SIRT1 overexpression decreased TLR4 expression, thereby repressing the phosphorylation of the NFκB subunit and p65 and decreasing ROS production.

conclusionsThese findings suggest that SIRT1 is a latent therapeutic target for mitigating LPS-induced inflammation via the TLR4-NFκB-ROS signaling axis.

Indexed as

CMLInflammationNFκBROSSIRT1TLR4

Identifiers

PMID32165863
PMCPMC7059700
OpenAlexW3010668768

What OpenQuestion holds

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Registered trials

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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.