Evidence map›Paper›PMID 33649847›Full record

ArticleMolecular medicine reports2021

Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway.

Hongwei Zhang, Fenqing Chi, Keru Qin, Xiuli Mu, Lieyang Wang, Bin Yang, Yanli Wang, Min Bai, Zhenhua Li, Liping Su and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 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

11 authors at 2 institutions in 1 country.

Hongwei Zhang *Department of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Fenqing Chi *Department of Biochemistry and Molecular Biology, Key Laboratory of Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Keru QinDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Xiuli MuDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Lieyang WangDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Bin YangDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Yanli WangDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Min BaiDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Zhenhua LiDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Liping SuDepartment of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China.
Baofeng YuDepartment of Biochemistry and Molecular Biology, Key Laboratory of Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.
Shanxi Provincial Cancer Hospital · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse large B‑cell lymphoma (DLBCL) is a highly heterogeneous malignant tumor type, and epigenetic modifications such as acetylation or deacetylation serve vital roles in its development. Chidamide, a novel histone deacetylase inhibitor, exerts an anticancer effect against various types of cancer. The present study aimed to evaluate the cellular effect of chidamide on a number of DLBCL cell lines and to investigate its underlying mechanism. The results demonstrated that chidamide induced the death of these cells in a concentration‑(0‑30 µmol/l) and time‑dependent (24‑72 h) manner, as determined using the Cell Counting Kit‑8 cell viability assay. Moreover, chidamide promoted cellular apoptosis, which was identified via flow cytometry and western blot analysis, with an increase in cleaved caspase‑3 expression and a decrease in Bcl‑2 expression. Chidamide treatment also decreased the expression level of STAT3 and its phosphorylation, which was accompanied by the downregulation of a class‑I histone deacetylase (HDAC) inhibitor, chidamide. Collectively, these data suggested that chidamide can be a potent therapeutic agent to treat DLBCL by inducing the apoptotic death of DLBCL cells by inhibiting the HDACs/STAT3/Bcl‑2 pathway.

Indexed as

AminopyridinesApoptosisBenzamidesCaspase 3Cell Line, TumorDose-Response Relationship, DrugGene ExpressionHistone Deacetylase InhibitorsHistone DeacetylasesHumansIsoenzymesLymphoma, Large B-Cell, DiffusePhosphorylationProto-Oncogene Proteins c-bcl-2Signal TransductionSTAT3 Transcription FactorAminopyridinesBCL2 protein, humanBenzamidesCaspase 3Histone Deacetylase InhibitorsHistone DeacetylasesIsoenzymesN-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamideProto-Oncogene Proteins c-bcl-2STAT3 protein, humanSTAT3 Transcription FactorapoptosisBcl‑2chidamideDLBCLHDACSTAT3

Identifiers

PMID33649847
PMCPMC7974270
OpenAlexW3134473644

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.