Evidence map›Paper›PMID 27508038›Full record

ArticleAmerican journal of translational research2016

Chidamide, a novel histone deacetylase inhibitor, inhibits the viability of MDS and AML cells by suppressing JAK2/STAT3 signaling.

Sida Zhao, Juan Guo, Youshan Zhao, Chengming Fei, Qingqing Zheng, Xiao Li, Chunkang Chang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.7field-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

46 citing papers in PubMed, 70 citations in OpenAlex.

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  7. The IRF2-INPP4B Pathway Aggravates Acute Myeloid LeukemiaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2025
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  11. Chidamide inhibits cell glycolysis in acute myeloid leukemia by decreasing N6-methyladenosine-related GNAS-AS1.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024
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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

7 authors at 1 institution in 1 country.

Sida ZhaoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Juan GuoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Youshan ZhaoDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Chengming FeiDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Qingqing ZhengDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Xiao LiDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Chunkang ChangDepartment of Hematology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital Shanghai, China.
Shanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have indicated that histone deacetylase (HDAC) activity is always increased in a lot of human tumors, and inhibition of HDAC activity is a promising new strategy in the treatment of cancers. Chidamide, a novel HDAC inhibitor of the benzamide class, is currently under clinical trials. In this study, we aimed to investigate the antitumor activity of Chidamide on myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) cell lines and explore the possible mechanism. Chidamide exhibited efficient anti-proliferative activity on MDS and AML cells in a time- and dose-dependent manner, accompanied by cell cycle arrest at G0/G1 phase and cell apoptosis. Importantly, Chidamide possessed potent HDAC inhibition property, as evaluated by HDAC activity analysis and acetylation of histone H3 and H4. Moreover, Chidamide significantly increased the expression of Suppressors of cytokine signaling 3 (SOCS3), reduced the expression of Janus activated kinases 2 (JAK2) and Signal transducer and activator of transcription 3 (STAT3), and inhibited STAT3 downstream genes, including c-Myc, Bcl-xL, and Mcl-1, which are involved in cell cycle progression and anti-apoptosis. Therefore, we demonstrate that Chidamide exhibits potent inhibitory effect on cell viability of MDS and AML cells, and the possible mechanism may lie in the downregulation of JAK2/STAT3 signaling through SOCS3 upregulation. Our data provide rationale for clinical investigations of Chidamide in MDS and AML.

Indexed as

acute myeloid leukemiaChidamidehistone deacetylase inhibitormyelodysplastic syndromesSTAT3

Identifiers

PMID27508038
PMCPMC4969454
OpenAlexW2512335901

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.