Evidence map›Paper›PMID 40791934›Full record

ArticleBlood science (Baltimore, Md.)2025

Alpha-enolase promotes progression of acute myeloid leukemia via MAPK/ERK signaling pathway.

Shanshan Zhang, Haina Wang, Xuehong Zhang, Xiangjie Kui, Dan Huang, Menglu Qin, Shuqing Liu, Ming-Zhong Sun, Jinsong Yan

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In one paragraph

Article in Blood science (Baltimore, Md.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shanshan ZhangDepartment of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Haina WangDepartment of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Xuehong ZhangCenter of Genome and Personalized Medicine, Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, China.
Xiangjie KuiDepartment of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Dan HuangDepartment of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Menglu QinLiaoning Key Laboratory of Hematopoietic Stem Cell Transplantation and Translational Medicine, Blood Stem Cell Transplantation Institute, Dalian Key Laboratory of hematology, Diamond Bay Institute of Hematology, the Second Hospital of Dalian Medical University, Dalian 116027, China.
Shuqing LiuDepartment of Biochemistry, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Ming-Zhong SunDepartment of Biotechnology, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, China.
Jinsong YanDepartment of Hematology, Liaoning Medical Center for Hematopoietic Stem Cell Transplantation, the Second Hospital of Dalian Medical University, Dalian 116027, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to the limited availability of effective treatment therapies, patients with refractory and relapsed acute myeloid leukemia (AML) often have poor prognoses. Therefore, identifying new therapeutic targets to improve the treatment landscape and enhance AML outcomes is critical. In this study, we demonstrated for the first time that alpha-enolase (ENO1) is markedly overexpressed in AML and is closely associated with poor prognosis. In vitro experiments revealed that ENO1 knockdown (shENO1) significantly inhibited cell proliferation and invasion, and concomitantly induced cell cycle arrest. In vivo, a mouse model engrafted with U937-shENO1 cells exhibited markedly prolonged overall survival compared with a model implanted with U937 cells. Mechanistically, ENO1 operates by activating the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway, as evidenced by the reversal of shENO1 function through ERK activation. Collectively, our findings highlight ENO1 as a promising therapeutic target in AML.

Indexed as

AMLENO1InvasionMAPK/ERK signaling pathwayProliferation

Identifiers

PMID40791934
PMCPMC12338211

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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.