Evidence map›Paper›PMID 26692928›Full record

ArticleAmerican journal of translational research2015

Matrine increases NKG2D ligand ULBP2 in K562 cells via inhibiting JAK/STAT3 pathway: a potential mechanism underlying the immunotherapy of matrine in leukemia.

Xuzhang Lu, Zhichao Zhu, Lijia Jiang, Xiao Sun, Zhuxia Jia, Sixuan Qian, Jianyong Li, Lingdi Ma

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  7. Small-Molecule Targets in Tumor Immunotherapy.Natural products and bioprospecting · 2018
    Review
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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

8 authors at 3 institutions in 1 country.

Xuzhang LuDepartment of Hematology, Changzhou NO. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University Changzhou 213000, China.
Zhichao ZhuLaboratory Center, Changzhou NO. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University Changzhou 213000, China.
Lijia JiangLaboratory Center, Changzhou NO. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University Changzhou 213000, China.
Xiao SunDepartment of Hematology, People Hospital of Jiangsu Province, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China.
Zhuxia JiaDepartment of Hematology, Changzhou NO. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University Changzhou 213000, China.
Sixuan QianDepartment of Hematology, People Hospital of Jiangsu Province, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China.
Jianyong LiDepartment of Hematology, People Hospital of Jiangsu Province, The First Affiliated Hospital of Nanjing Medical University Nanjing 210029, China.
Lingdi MaDepartment of Laboratory Medicine, Huizhou NO. 3 People's Hospital, Affiliated Hospital of Guangzhou Medical University Huizhou 615000, China.
Changzhou No.2 People's Hospital · CNNanjing Medical University · CNHuizhou Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe study aimed to investigate the role of the JAK/STAT3 pathway in the matrine induced ULBP2 expression on the human chronic myelogenous leukemia K562 cells.

methodsK562 cells were cultured, and the relevant mRNA expressions were detected.

resultsMatrine induced the expression of four NKG2D ligands on K562 cells, of which ULBP2 had the highest increase. After treatment with 0.8 mg/mL matrine for 24 h, the mean fluorescence intensity (MFI) of ULBP2 increased. After matrine treatment, the sensitivity of K562 cells to NK cell-mediated killing increased significantly. After treatment with 0.2, 0.5 and 0.8 mg/ mL matrine, the percentage of K562 cells killed by NK cells was significantly higher than that of untreated cells (29.2%) (P<0.05). Matrine significantly inhibit the protein expression of phosphorylated STAT 3 and JAK2. Matrine markedly inhibited the IL-6 expression of K562 cells, and antagonized the IL-6 mediated STAT3 and JAK2 phosphorylation. In addition, matrine enhanced the inhibitory effect of STAT 3 inhibitor on STAT 3 activity. The silencing of STAT expression and inhibition of STAT3 activity significantly up-regulated the ULPB2 expression. Matrine had no effect on the expression of IL-6R and gp130 on K562 cells, the mRNA expression of IL-6R and gp130 increased slightly and the sgp 130 in cell supernatant significantly increased.

conclusionsOur findings reveal IL-6 and IL-6 receptor-mediated JAK/STAT3 pathway is involved in the matrine induced up-regulation of NKG2D ligands ULBP2 on K562 cells. Matrine might inhibit IL-6 expression and then suppress the activation of IL-6 receptor-mediated JAK/STAT3 pathway.

Indexed as

IL-6K562 cellsMatrineNK cellsNKG2D ligandSTAT3

Identifiers

PMID26692928
PMCPMC4656761
OpenAlexW2403541567

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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.