Evidence map›Paper›PMID 37131085›Full record

ArticleFrontiers of medicine2023

ACSL5, a prognostic factor in acute myeloid leukemia, modulates the activity of Wnt/β-catenin signaling by palmitoylation modification.

Wenle Ye, Jinghan Wang, Jiansong Huang, Xiao He, Zhixin Ma, Xia Li, Xin Huang, Fenglin Li, Shujuan Huang, Jiajia Pan and 6 more

Abstract read
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Article in Frontiers of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 17 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

16 authors at 4 institutions in 2 countries.

Wenle Ye *Department of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Jinghan Wang *Department of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Jiansong HuangDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Xiao HeResearch Centre, Centre hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, H2L 4M1, Canada.
Zhixin MaWomen's Hospital, School of Medicine, Zhejiang University, Hangzhou, 310006, China.
Xia LiDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Xin HuangDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Fenglin LiDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Shujuan HuangDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Jiajia PanDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Jingrui JinDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Qing LingDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Yungui WangDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China.
Yongping YuZhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, China.
Jie SunDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China. sunjiehm@zju.edu.cn.
Jie JinDepartment of Hematology, The First Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, 310003, China. jiej0503@zju.edu.cn.
First Affiliated Hospital Zhejiang University · CNCentre Hospitalier de l’Université de Montréal · CAWomen's Hospital, School of Medicine, Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acyl-CoA synthetase long chain family member 5 (ACSL5), is a member of the acyl-CoA synthetases (ACSs) family that activates long chain fatty acids by catalyzing the synthesis of fatty acyl-CoAs. The dysregulation of ACSL5 has been reported in some cancers, such as glioma and colon cancers. However, little is known about the role of ACSL5 in acute myeloid leukemia (AML). We found that the expression of ACSL5 was higher in bone marrow cells from AML patients compared with that from healthy donors. ACSL5 level could serve as an independent prognostic predictor of the overall survival of AML patients. In AML cells, the ACSL5 knockdown inhibited cell growth both in vitro and in vivo. Mechanistically, the knockdown of ACSL5 suppressed the activation of the Wnt/β-catenin pathway by suppressing the palmitoylation modification of Wnt3a. Additionally, triacsin c, a pan-ACS family inhibitor, inhibited cell growth and robustly induced cell apoptosis when combined with ABT-199, the FDA approved BCL-2 inhibitor for AML therapy. Our results indicate that ACSL5 is a potential prognosis marker for AML and a promising pharmacological target for the treatment of molecularly stratified AML.

Indexed as

Leukemia, Myeloid, AcuteAntineoplastic AgentsApoptosisbeta CateninBiomarkers, TumorCell Line, TumorCoenzyme A LigasesHumansLipoylationPrognosisWnt Signaling PathwayACSL5 protein, humanAntineoplastic Agentsbeta CateninBiomarkers, TumorCoenzyme A LigasesABT-199acute myeloid leukemiaacyl-CoA synthetase long chain family member 5palmitoylationWnt3a

Identifiers

PMID37131085
OpenAlexW4367669897

What OpenQuestion holds

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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.