Evidence map›Paper›PMID 29891507›Full record

ArticleCancer research2018

Aberrant FGFR Tyrosine Kinase Signaling Enhances the Warburg Effect by Reprogramming LDH Isoform Expression and Activity in Prostate Cancer.

Junchen Liu, Guo Chen, Zezhen Liu, Shaoyou Liu, Zhiduan Cai, Pan You, Yuepeng Ke, Li Lai, Yun Huang, Hongchang Gao and 8 more

Abstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

89 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
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  13. Article
  14. A Novel Autophagy InhibitorResearch (Washington, D.C.) · 2026
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  15. Review
  16. Review
  17. Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025
    Review
  18. Article
  19. Article
  20. Inhibition Profiling ofMolecules (Basel, Switzerland) · 2025
    Article

29 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 6 institutions in 2 countries.

Junchen Liu *Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China.
Guo Chen *Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China.
Zezhen Liu *Department of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China.
Shaoyou LiuDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China.
Zhiduan CaiDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China.
Pan YouXianyue Hospital, Xiamen, China.
Yuepeng KeInstitute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, Texas.
Li LaiInstitute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, Texas.
Yun HuangInstitute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, Texas.
Hongchang GaoWenzhou Medical University, Wenzhou, China.
Liangcai ZhaoWenzhou Medical University, Wenzhou, China.
Helene PelicanoDepartments of Translational Molecular Pathology, MD Anderson Cancer Center, Houston, Texas.
Peng HuangDepartments of Translational Molecular Pathology, MD Anderson Cancer Center, Houston, Texas.
Wallace L McKeehanInstitute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, Texas.
Chin-Lee WuDepartments of Pathology and Urology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Cong WangWenzhou Medical University, Wenzhou, China. fwang@ibt.tamhsc.edu zhongwd2009@live.cn cwang@wmu.edu.cn.
Weide ZhongDepartment of Urology, Guangdong Key Laboratory of Clinical Molecular Medicine and Diagnostics, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China. fwang@ibt.tamhsc.edu zhongwd2009@live.cn cwang@wmu.edu.cn.
Fen WangInstitute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, Texas. fwang@ibt.tamhsc.edu zhongwd2009@live.cn cwang@wmu.edu.cn.
Second Affiliated Hospital of Guangzhou Medical University · CNTexas A&M University · USWenzhou Medical University · CNThe University of Texas MD Anderson Cancer Center · US174th hospital of the People's Liberation Army · CNMassachusetts General Hospital · US

Funding

Receptor-specific signaling of FGFR in the prostateR01CA096824 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI WANG, FEN · 2003 to 2013
$2.5M
FRS2-mediated Signals in Prostatic Tumorigenesis and DevelopmentR56CA096824 · NCI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI WANG, FEN · 2008 to 2008
$302k
NCI NIH HHS R01 CA096824NCI NIH HHS R56 CA096824
6 · The paper itself

Abstract

The acquisition of ectopic fibroblast growthfactor receptor 1 (FGFR1) expression is well documented in prostate cancer progression. How it contributes to prostate cancer progression is not fully understood, although it is known to confer a growth advantage and promote cell survival. Here, we report that FGFR1 tyrosine kinase reprograms the energy metabolism of prostate cancer cells by regulating the expression of lactate dehydrogenase (LDH) isozymes. FGFR1 increased LDHA stability through tyrosine phosphorylation and reduced LDHB expression by promoting its promoter methylation, thereby shifting cell metabolism from oxidative phosphorylation to aerobic glycolysis. LDHA depletion compromised, whereas LDHB depletion enhanced the tumorigenicity of prostate cancer cells. Furthermore, FGFR1 overexpression and aberrant LDH isozyme expression were associated with short overall survival and biochemical recurrence times in patients with prostate cancer. Our results indicate that ectopic FGFR1 expression reprograms the energy metabolism of prostate cancer cells, representing a hallmark change in prostate cancer progression.

Indexed as

Carcinogenicity TestsCell ProliferationCell SurvivalCellular ReprogrammingGene Expression Regulation, NeoplasticHumansLactate DehydrogenasesL-Lactate DehydrogenaseMaleProstatic NeoplasmsProtein IsoformsProtein StabilityReceptor, Fibroblast Growth Factor, Type 1Signal TransductionD-lactate dehydrogenaseLactate DehydrogenasesLDHA protein, humanL-Lactate DehydrogenaseProtein IsoformsReceptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID29891507
PMCPMC6095720
OpenAlexW2807936922

What OpenQuestion holds

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LicenceTDM
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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.