Evidence map›Paper›PMID 36774517›Full record

ArticleJournal of translational medicine2023

Spermatogenesis associated serine rich 2 like plays a prognostic factor and therapeutic target in acute myeloid leukemia by regulating the JAK2/STAT3/STAT5 axis.

Fenglin Li, Wenle Ye, Yiyi Yao, Wenwen Wei, Xiangjie Lin, Haihui Zhuang, Chenying Li, Xia Li, Qing Ling, Chao Hu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.7field-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

7 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

16 authors at 3 institutions in 1 country.

Fenglin Li *Department of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Wenle Ye *Department of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Yiyi Yao *Department of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Wenwen WeiDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Xiangjie LinDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Haihui ZhuangDepartment of Hematology, The Affiliated People's Hospital of Ningbo University, Baizhang road 251#, Ningbo, China.
Chenying LiDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Xia LiDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Qing LingDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Chao HuDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Xin HuangDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Yu QianDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Shihui MaoDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Jiansong HuangDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China.
Ying LuDepartment of Hematology, The Affiliated People's Hospital of Ningbo University, Baizhang road 251#, Ningbo, China. rmluying@nbu.edu.cn.
Jie JinDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Qingchun road 79#, Hangzhou, China. jiej0503@zju.edu.cn.ORCID 0000-0002-8166-9915
Zhejiang University · CNNingbo University · CNZhejiang Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSpermatogenesis associated serine rich 2 like (SPATS2L) was highly expressed in homoharringtonine (HHT) resistant acute myeloid leukemia (AML) cell lines. However, its role is little known in AML. The present study aimed to investigate the function of SPATS2L in AML pathogenesis and elucidate the underlying molecular mechanisms.

methodsOverall survival (OS), event-free survival (EFS), relapse-free survival (RFS) were used to evaluate the prognostic impact of SPATS2L for AML from TCGA database and ourcohort. ShRNA was used to knockdown the expression of SPATS2L. Apoptosis was assessed by flow cytometry. The changes of proteins were assessed by Western blot(WB). A xenotransplantation mice model was used to evaluate in vivo growth and survival. RNA sequencing was performed to elucidate the molecular mechanisms underlying the role of SPATS2L in AML.

resultsSPATS2L expression increased with increasing resistance indexes(RI) in HHT-resistant cell lines we had constructed. Higher SPATS2L expression was observed in intermediate/high-risk patients than in favorable patients. Meanwhile, decreased SPATS2L expression was observed in AML patients achieving complete remission (CR). Multivariate analysis showed high SPATS2L expression was an independent poor predictor of OS, EFS, RFS in AML. SPATS2L knock down (KD) suppressed cell growth, induced apoptosis, and suppressed key proteins of JAK/STAT pathway, such as JAK2, STAT3, STAT5 in AML cells. Inhibiting SPATS2L expression markedly enhanced the pro-apoptotic effects of traditional chemotherapeutics (Ara-c, IDA, and HHT).

conclusionsHigh expression of SPATS2L is a poor prognostic factor in AML, and targeting SPATS2L may be a promising therapeutic strategy for AML patients.

Indexed as

Leukemia, Myeloid, AcuteSTAT5 Transcription FactorAnimalsHomoharringtonineHumansJanus KinasesMicePrognosisProteinsSignal TransductionSTAT Transcription FactorsHomoharringtonineJanus KinasesProteinsSPATS2L protein, humanSTAT5 Transcription FactorSTAT Transcription FactorsAMLApoptosisGrowthJAK/STAT pathwayPrognosticSPATS2LTherapeutic target

Identifiers

PMID36774517
PMCPMC9921581
OpenAlexW4320038685

What OpenQuestion holds

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LicenceCC BY
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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.