Evidence map›Paper›PMID 35116779›Full record

ArticleTranslational cancer research2019

Rapamycin downregulates NKG2D ligands in acute myeloid leukemia cells via an activation of the STAT3 pathway: a potential mechanism for rapamycin-induced immune escape in leukemia.

Zhichao Zhu, Yu Bai, Xuzhang Lu, Jun Ding, Chunjian Qi

Open access · diamondAbstract read
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Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

5 citing papers in PubMed, 8 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 2 institutions in 1 country.

Zhichao ZhuMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Yu BaiMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Xuzhang LuDepartment of Hematology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Jun DingMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Chunjian QiMedical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou 213003, China.
Changzhou No.2 People's Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe constitutive activation of the mammalian target of rapamycin (mTOR) is involved in the pathogenesis of many cancers. Rapamycin (RAPA), a specific inhibitor of mTOR, has been applied to the clinical treatment of tumors, and its anti-leukemia effect has also been confirmed.

methodsWe detected apoptosis and the NKG2D ligands expression in acute myeloid leukemia (AML) cells using flow cytometry and investigated the cytotoxicity of AML cells that had been co-cultured with natural killer (NK) cells using CFSE staining. We evaluated the signal pathways with a western blot assay.

resultsIn this study, we found that RAPA can significantly inhibit the proliferation of AML cells. Further studies showed that the use of RAPA alone reduced the expression of NKG2D ligands on the membranes of HL-60 and THP-1 AML cells. Also, RAPA blocked the upregulation of the NKG2D ligand when AML cells were cultured with the demethylation drug decitabine (DAC). We found that RAPA decreased the expression of the NKG2D ligands by inducing the STAT3 phosphorylation of AML cells.

conclusionsThe discovery of this mechanism might further optimize the clinical use of RAPA for the treatment of AML.

Indexed as

acute myeloid leukemia (AML)immune escapeNKG2D ligandRapamycin (RAPA)STAT3

Identifiers

PMID35116779
PMCPMC8798175
OpenAlexW4239141776

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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.