Evidence map›Paper›PMID 25619392›Full record

ArticleActa pharmacologica Sinica2015

Resveratrol induces apoptosis of human chronic myelogenous leukemia cells in vitro through p38 and JNK-regulated H2AX phosphorylation.

Xin-pin Wu, Min Xiong, Cheng-shan Xu, Lian-ning Duan, Ya-qiong Dong, Yuan Luo, Tian-hui Niu, Cheng-rong Lu

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 57 citations in OpenAlex.

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  12. International journal of molecular sciences · 2021
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  14. Potential ApproachesFrontiers in oncology · 2021
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  15. Article
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  19. The Anti-Cancer Effect ofAntioxidants (Basel, Switzerland) · 2019
    Article
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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 2 institutions in 1 country.

Xin-pin Wu1] Clinical School of Air Force General Hospital, Anhui Medical University, Heifei 230000, China [2] Aviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Min XiongAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Cheng-shan XuAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Lian-ning DuanAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Ya-qiong DongAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Yuan LuoAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Tian-hui NiuAviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Cheng-rong Lu1] Clinical School of Air Force General Hospital, Anhui Medical University, Heifei 230000, China [2] Aviation Medicine Research Laboratory, Air Force General Hospital, PLA, Beijing 100142, China.
Air Force General Hospital PLA · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe phosphorylation of histone H2AX, a novel tumor suppressor protein, is involved in regulation of cancer cell apoptosis. The aim of this study was to examine whether H2AX phosphorylation was required for resveratrol-induced apoptosis of human chronic myelogenous leukemia (CML) cells in vitro.

methodsK562 cells were tested. Cell apoptosis was analyzed using flow cytometry, and the phosphorylation of H2AX and other signaling proteins was examined with Western blotting. To analyze the signaling pathways, the cells were transfected with lentiviral vectors encoding H2AX-wt or specific siRNAs.

resultsTreatment of K562 cells with resveratrol (20-100 μmol/L) induced apoptosis and phosphorylation of H2AX at Ser139 in time- and dose-dependent manners, but reduced phosphorylation of histone H3 at Ser10. Resveratrol treatment activated two MAPK family members p38 and JNK, and blocked the activation of another MAPK family member ERK. Pretreatment with the p38 inhibitor SB202190 or the JNK inhibitor SP600125 dose-dependently reduced resveratrol-induced phosphorylation of H2AX, which were also observed when the cells were transfected with p38- or JNK-specific siRNAs. Overexpression of H2AX in K562 cells markedly increased resveratrol-induced apoptosis, whereas overexpression of H2AX-139m (Ser139 was mutated to block phosphorylation) inhibited resveratrol-induced apoptosis. K562 cells transfected with H2AX-specific siRNAs were resistant to resveratrol-induced apoptosis.

conclusionH2AX phosphorylation at Ser139 in human CML cells, which is regulated by p38 and JNK, is essential for resveratrol-induced apoptosis.

Indexed as

Antineoplastic AgentsApoptosisDose-Response Relationship, DrugHistonesHumansJNK Mitogen-Activated Protein KinasesK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL Positivep38 Mitogen-Activated Protein KinasesPhosphorylationProtein Kinase InhibitorsResveratrolRNA InterferenceSignal TransductionStilbenesTime FactorsAntineoplastic AgentsH2AX protein, humanHistonesJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsResveratrolStilbenes

Identifiers

PMID25619392
PMCPMC4349923
OpenAlexW1970390048

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.