Evidence map›Paper›PMID 22388075›Full record

ArticleActa pharmacologica Sinica2012

Imatinib induces H2AX phosphorylation and apoptosis in chronic myelogenous leukemia cells in vitro via caspase-3/Mst1 pathway.

Yan-jun Zhang, Cheng-rong Lu, Yan Cao, Yuan Luo, Rong-feng Bao, Shu Yan, Mei Xue, Feng Zhu, Zhe Wang, Lian-ning Duan

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 45 citations in OpenAlex.

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  8. The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021
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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

10 authors at 4 institutions in 2 countries.

Yan-jun ZhangAviation Medicine Research Lab, General Hospital of Air Force, Beijing, China.
Cheng-rong Lu
Yan Cao
Yuan Luo
Rong-feng Bao
Shu Yan
Mei Xue
Feng Zhu
Zhe Wang
Lian-ning Duan
Air Force General Hospital PLA · CNChina Medical University · CNHebei North University · CNHormel (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimHistone H2AX is a novel tumor suppressor and its phosphorylation at the C terminus (Ser139 and Tyr142) is required for tumor cell apoptosis. The aim of the present study was to elucidate the mechanisms underlying imatinib-induced C-terminal phosphorylation of H2AX in chronic myelogenous leukemia cells in vitro.

methodsBCR-ABL-positive K562 cells were used. Microscopy, Western blotting and flow cytometry were used to study the signaling pathways that regulate imatinib-induced H2AX phosphorylation and the apoptotic mechanisms.

resultsTreatment of K562 cells with imatinib (1-8 μmol/L) induced phosphorylation of H2AX at Ser139 and Tyr142 in time- and dose-dependent manners. In contrast, imatinib at the same concentrations did not affect H2AX acetylation at Lys 5, and the acetylated H2AX maintained a higher level in the cells. Meanwhile, imatinib (1-8 μmol/L) activated caspase-3 and its downstream mammalian STE20-like kinase 1 (Mst1), and induced apoptosis of K562 cells. The caspase-3 inhibitor Z-VAD (40 μmol/L) reduced imatinib-induced H2AX phosphorylation at Ser139 and Tyr142 and blocked imatinib-induced apoptosis of K562 cells. Imatinib (4 μmol/L) induced expression of Williams-Beuren syndrome transcription factor (WSTF), but not wild-type p53-induced phosphatase 1 (Wip1) in K562 cells.

conclusionThe caspase-3/Mst1 pathway is required for H2AX C-terminal phosphorylation at Ser139 and Tyr142 and subsequent apoptosis in Bcr-Abl-positive K562 cells induced by imatinib.

Indexed as

Antineoplastic AgentsApoptosisBenzamidesCaspase 3Cell Line, TumorHepatocyte Growth FactorHistonesHumansImatinib MesylateLeukemia, Myelogenous, Chronic, BCR-ABL PositivePhosphorylationPiperazinesProto-Oncogene ProteinsPyrimidinesSignal TransductionAntineoplastic AgentsBenzamidesCaspase 3H2AX protein, humanHepatocyte Growth FactorHistonesImatinib Mesylatemacrophage stimulating proteinPiperazinesProto-Oncogene ProteinsPyrimidines

Identifiers

PMID22388075
PMCPMC4003371
OpenAlexW1996890993

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.