Evidence map›Paper›PMID 40380235›Full record

ArticleCell & bioscience2025

The HNRNPC/CELF2 signaling pathway drives glycolytic reprogramming and mitochondrial dysfunction in drug-resistant acute myeloid leukemia.

Xiang Ma, Haodong Li, Ziqi Zhao, Changchun Li, Man Wang, Lele Zhang, Yutong Zhao, Haipeng Su, Feng Wang, Jiai Hua

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Article
  2. Review
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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

10 authors.

Xiang MaLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Haodong LiLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Ziqi ZhaoChemistry and Chemical Engineering Department, Taiyuan Institute of Technology, Taiyuan, 030008, People's Republic of China.
Changchun LiChemistry and Chemical Engineering Department, Taiyuan Institute of Technology, Taiyuan, 030008, People's Republic of China.
Man WangLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Lele ZhangLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Yutong ZhaoLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Haipeng SuLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China.
Feng WangChemistry and Chemical Engineering Department, Taiyuan Institute of Technology, Taiyuan, 030008, People's Republic of China.
Jiai HuaLaboratory of Biochemistry and Pharmacy, Taiyuan Institute of Technology, No. 31, Xinlan Road, Jiancaoping District, Taiyuan, 030008, Shanxi, People's Republic of China. huaja@tit.edu.cn.

Funding

Shanxi Province Science Foundation 20210302124333
6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is an aggressive cancer with high treatment resistance, often leading to poor patient outcomes. Metabolic reprogramming plays a critical role in AML progression, influencing drug resistance (DR) and tumor survival. This study investigates the HNRNPC/CELF2 signaling pathway and its impact on AML cell metabolism and DR.

resultsThe study identified that HNRNPC regulates the expression of CELF2 through m6 A modification. In drug-resistant AML cells, increased HNRNPC expression and decreased CELF2 expression were associated with upregulated glycolysis, enhanced glucose consumption, lactate production, and mitochondrial dysfunction. Knockdown of HNRNPC reduced glycolysis and cell invasion, while CELF2 knockdown reversed these effects. Conversely, HNRNPC overexpression enhanced glycolysis and cell migration, which were counteracted by CELF2 overexpression.

conclusionsThe HNRNPC/CELF2 axis plays a pivotal role in metabolic reprogramming, driving AML progression and chemotherapy resistance. Targeting this pathway may offer new therapeutic strategies to overcome resistance and improve treatment outcomes in AML patients.

Indexed as

Acute myeloid leukemiaCell migrationCUGBP elav-like family member 2Drug resistanceGlucose metabolism reprogrammingHeterogeneous nuclear ribonucleoprotein C

Identifiers

PMID40380235
PMCPMC12083169

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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.