Evidence map›Paper›PMID 24585095›Full record

ArticleInternational journal of oncology2014

Spautin-1, a novel autophagy inhibitor, enhances imatinib-induced apoptosis in chronic myeloid leukemia.

Shan Shao, Su Li, Youwen Qin, Xiaorui Wang, Yining Yang, Haitao Bai, Lili Zhou, Chuxian Zhao, Chun Wang

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 2 pooled it
5.8field-weighted citation impact, top 3% 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

92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 150 citations in OpenAlex.

  1. The multiple roles of autophagy in uveal melanoma and the microenvironment.Journal of cancer research and clinical oncology · 2024
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  15. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
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32 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Shan ShaoDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Su LiDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Youwen QinDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Xiaorui WangDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Yining YangDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Haitao BaiDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Lili ZhouDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Chuxian ZhaoDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Chun WangDepartment of Hematology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.
Shanghai First People's Hospital · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

Imatinib mesylate (IM), a targeted competitive inhibitor of the BCR-ABL tyrosine kinase, has revolutionized the clinical treatment of chronic myeloid leukemia (CML). However, resistance and intolerance are still a challenge in the treatment of CML. Autophagy has been proposed to play a role in IM resistance. To investigate the anti-leukemic activity of specific and potent autophagy inhibitor-1 (spautin-1) in CML, we detected its synergistic effect with IM in K562 and CML cells. Our results showed that spautin-1 markedly inhibited IM-induced autophagy in CML cells by downregulating Beclin-1. Spautin-1 enhanced IM-induced CML cell apoptosis by reducing the expression of the anti-apoptotic proteins Mcl-1 and Bcl-2. We further demonstrated that the pro-apoptotic activity of spautin-1 was associated with activation of GSK3β, an important downstream effector of PI3K/AKT. The findings indicate that the autophagy inhibitor spautin-1 enhances IM-induced apoptosis by inactivating PI3K/AKT and activating downstream GSK3β, leading to downregulation of Mcl-1 and Bcl-2, which represents a promising approach to improve the efficacy of IM in the treatment of patients with CML.

Indexed as

Antineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1BenzamidesBenzylaminesDrug Resistance, NeoplasmDrug SynergismGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansImatinib MesylateK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveAntineoplastic AgentsApoptosis Regulatory ProteinsBeclin-1BECN1 protein, humanBenzamidesBenzylaminesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanImatinib MesylateMCL1 protein, humanMembrane ProteinsMyeloid Cell Leukemia Sequence 1 ProteinPiperazinesPyrimidinesQuinazolinesspautin-1

Identifiers

PMID24585095
PMCPMC6904104
OpenAlexW1977079962

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.