Evidence map›Paper›PMID 41244129›Full record

ReviewAmerican journal of cancer research2025

Hexokinase 2 promotes tumor development and progression.

Guojuan Wang, Yujuan Lai, Xiudan Chen, Nanxin Li, Chen Zhong, Yuwei Yan, Qingqing Ma, Xinlin Hong, Naicheng Zhu, Wenyan Yu

Abstract readReview
In one paragraph

Review in American journal of cancer research, 2025. 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
–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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
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.

Guojuan WangAffiliated Hospital of Jiangxi University of Chinese Medicine Nanchang 330006, Jiangxi, China.
Yujuan LaiAffiliated Hospital of Jiangxi University of Chinese Medicine Nanchang 330006, Jiangxi, China.
Xiudan ChenResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Nanxin LiResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Chen ZhongResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Yuwei YanResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Qingqing MaResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Xinlin HongResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Naicheng ZhuResearch Center for Differentiation and Development of TCM Basic Theory, Discipline of Chinese and Western Integrative Medicine, Jiangxi University of Chinese Medicine, Jiangxi Key Laboratory of Etiology and Biology of TCM Nanchang 330004, Jiangxi, China.
Wenyan YuAffiliated Hospital of Jiangxi University of Chinese Medicine Nanchang 330006, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer remains a leading cause of morbidity and mortality worldwide, and the abnormal activation of glycolysis is a hallmark that enables tumor cells to adapt and sustain rapid proliferation. Beyond providing energy and biosynthetic precursors, glycolysis also supports tumor cell survival, invasion, and metastasis through multiple mechanisms. Hexokinase is a key rate-limiting enzyme in glycolysis, catalyzing the phosphorylation of glucose to glucose-6-phosphate. Among its isoforms, hexokinase 2 (HK2) exhibits particularly high enzymatic activity and substrate specificity, and it plays a central role in tumor metabolic reprogramming. Recent studies have shown that HK2 is markedly upregulated in many cancer types, where it promotes tumor initiation and progression by suppressing apoptosis and enhancing proliferation and metastasis. This review summarizes current evidence on the role of HK2 in tumor development and discusses emerging therapeutic strategies targeting HK2. By clarifying the link between HK2 and cancer, we aim to provide new insights and potential clinical applications for metabolism-based therapies.

Indexed as

apoptosisdrug resistanceHexokinase 2proliferationtumor metabolismWarburg effect

Identifiers

PMID41244129
PMCPMC12616175

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.