Evidence map›Paper›PMID 36621846›Full record

ArticleCancer medicine2023

Dihydropyrimidinase-like 2 can serve as a novel therapeutic target and prognostic biomarker in acute myeloid leukemia.

Fenglin Li, Qing Ling, Jiaying Lian, Ying Chen, Chao Hu, Min Yang, Xiang Zhang, Chenying Li, Shihui Mao, Wenle Ye and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

5 citing papers in PubMed, 13 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

19 authors at 3 institutions in 1 country.

Fenglin LiDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Qing LingDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Jiaying LianDepartment of Hematology, The affiliated people's hospital of Ningbo University, Ningbo, China.
Ying ChenDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Chao HuDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Min YangDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Xiang ZhangDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Chenying LiDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Shihui MaoDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Wenle YeDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Xia LiDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Xiangjie LinDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Wenwen WeiDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Xin HuangDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Jiajia PanDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Yu QianDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Jinghan WangDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.ORCID 0000-0002-7210-4824
Ying LuDepartment of Hematology, The affiliated people's hospital of Ningbo University, Ningbo, China.ORCID 0000-0003-2960-3131
Jie JinDepartment of Hematology, the First Affiliated Hospital, Zhejiang University, College of Medicine, Hangzhou, Zhejiang, People's Republic of China.ORCID 0000-0002-8166-9915
Hangzhou First People's Hospital · CNNingbo University · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdentifying therapeutic targets and prognostic biomarkers significantly contributes to individualized treatment of acute myeloid leukemia (AML). Dihydropyrimidinase-like 2 (DPYSL2) expression was decreased in homoharringtonine (HHT)-resistant AML cells, which were established by our group. DPYSL2 plays an important role in axon growth and has oncogene effect in glioblastoma. However, little research has been conducted to investigate the function of DPYSL2 in AML pathogenesis.

methodsAuto-docking was used to reveal the targeting relationship between HHT and DPYSL2. Overall survival (OS), event-free survival (EFS), and relapse-free survival (RFS) were used to evaluate the prognostic impact of DPYSL2 for AML. ShRNA was used to knockdown the expression of SPATS2L. Apoptosis was assessed by flow cytometry. In vivo growth and survival were assessed using a xenotransplantation mice model. RNA sequencing was performed to elucidate the molecular mechanisms underlying the role of SPATS2L in AML and were confirmed by Western blot.

resultsWe found DPYSL2 was the target of HHT. Next, we found AML cell lines and patients had higher DPYSL2 expression levels than the normal samples. Further multivariate analysis demonstrated that high DPYSL2 expression was an independent poor prognostic factor for OS, EFS, and RFS in AML. Inhibition of DPYSL2 expression suppressed cell growth, induced apoptosis in AML cell lines, and prolonged the survival of AML xenograft NCG mice. Through RNA-seq analysis from TCGA and our data, the JAK2/STAT3/STAT5-PI3K P85/AKT/GSK3b axis was thought to be the critical pathway in regulating DPYSL2 in AML development.

conclusionsWe first time confirmed that DPYSL2 was a target of HHT and played an oncogene role in AML by regulating JAK/STAT signaling pathway. Therefore, DPYSL2 could serve as a novel prognostic marker and therapeutic target for AML treatment.

Indexed as

Leukemia, Myeloid, AcuteAmidohydrolasesAnimalsBiomarkersCell Line, TumorHomoharringtonineHumansMicePrognosisAmidohydrolasesBiomarkersdihydropyrimidinaseHomoharringtonineAMLbiomarkerDPYSL2HHTPI3K/Aktprognostic

Identifiers

PMID36621846
PMCPMC10134331
OpenAlexW4313880188

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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.