Evidence map›Paper›PMID 38066391›Full record

ArticleApoptosis : an international journal on programmed cell death2024

Synergistic cytotoxicity of decitabine and YM155 in leukemia cells through upregulation of SLC35F2 and suppression of MCL1 and survivin expression.

Jing-Ting Chiou, Long-Sen Chang

Abstract read
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In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 12 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

2 authors at 1 institution in 1 country.

Jing-Ting ChiouInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, 804, Taiwan.
Long-Sen ChangInstitute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, 804, Taiwan. lschang@mail.nsysu.edu.tw.
National Sun Yat-sen University · TW

Funding

National Science and Technology Council, Taiwan NSTC112-2320-B110-003
6 · The paper itself

Abstract

The hypomethylation agent decitabine (DAC), in combination with other apoptosis inducers, is considered a potential modality for cancer treatment. We investigated the mechanism underlying the combined cytotoxicity of DAC and YM155 in acute myeloid leukemia (AML) cells because of increasing evidence that YM155 induces apoptosis in cancer cells. Co-administration of DAC and YM155 resulted in synergistic cytotoxicity in AML U937 cells, which was characterized by the induction of apoptosis, NOXA-dependent degradation of MCL1 and survivin, and depolarization of mitochondria. Restoration of MCL1 or survivin expression attenuated DAC/YM155-induced U937 cell death. DAC initiated AKT and p38 MAPK phosphorylation in a Ca

Indexed as

Leukemia, Myeloid, AcuteMembrane Transport ProteinsNaphthoquinonesApoptosisCell Line, TumorDecitabineHumansInhibitor of Apoptosis ProteinsMyeloid Cell Leukemia Sequence 1 Proteinp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktSurvivinU937 CellsUp-RegulationDecitabineInhibitor of Apoptosis ProteinsMCL1 protein, humanMembrane Transport ProteinsMyeloid Cell Leukemia Sequence 1 ProteinNaphthoquinonesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktSLC35F2 protein, humanSurvivinAcute myeloid leukemiaDecitabineMCL1 and survivin degradationSLC35F2Synergistic cytotoxicityYM155

Identifiers

PMID38066391
OpenAlexW4389490841

What Socratic 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 Socratic graph.