Evidence map›Paper›PMID 32274668›Full record

ArticleDigestive diseases and sciences2021

Androgen Receptor Stimulates Hexokinase 2 and Induces Glycolysis by PKA/CREB Signaling in Hepatocellular Carcinoma.

R F Sun, C Y Zhao, S Chen, W Yu, M M Zhou, C R Gao

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Emerging roles and the regulation of aerobic glycolysis in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2020
    Review
  17. 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

6 authors.

R F Sun *Department of Pathology, School of Forensic Medicine, Shanxi Medical University, 29 Jiefangnan Road, Taiyuan, 030001, Shanxi Province, China.
C Y Zhao *School of Nursing, Taihu University of Wuxi, Wuxi, Jiangsu Province, China.
S ChenSchool of Nursing, Taihu University of Wuxi, Wuxi, Jiangsu Province, China.
W YuSchool of Nursing, Taihu University of Wuxi, Wuxi, Jiangsu Province, China.
M M ZhouSchool of Nursing, Taihu University of Wuxi, Wuxi, Jiangsu Province, China.
C R GaoDepartment of Pathology, School of Forensic Medicine, Shanxi Medical University, 29 Jiefangnan Road, Taiyuan, 030001, Shanxi Province, China. 1000128671@163.com.

Funding

National Natural Science Foundation of China 81971790
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) escapes growth inhibition by upregulating hexokinase 2 (HK2); however, the mechanism by which tumor cells upregulate HK2 remains unclear.

aimWe aimed to investigate the role of androgen receptor (AR) signalling in promoting HK2 expression in HCC.

methodsThe expressions of AR and HK2 in HCC tissues were analyzed by immunohistochemistry. Cell proliferation was determined using the CCK-8 assay, and the molecular mechanism of AR in the regulation of HK2 was evaluated by immunoblotting and luciferase assays.

resultsAR expression is positively correlated with HK2 staining by an immunohistochemical analysis. The manipulation of AR expression changed HK2 expression and glycolysis. AR signaling promoted the growth of HCC by enhancing HK2-mediated glycolysis. Moreover, AR stimulated HK2 levels and glycolysis by potentiating protein kinase A/cyclic adenosine monophosphate response element-binding (CREB) protein signaling. CREB silencing decreased HK2 expression and inhibited AR-mediated HCC glycolysis. AR affected the sensitivity of HCC cells to glycolysis inhibitors by regulating downstream phosphorylated (p)-CREB.

conclusionsThese results indicate that AR at least partially induced glycolysis via p-CREB regulation of HK2 in HCC cells. Thus, this pathway should be considered for the design of novel therapeutic methods to target AR-overexpressing HCC.

Indexed as

Carcinoma, HepatocellularCell ProliferationCells, CulturedCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinGene Expression Regulation, NeoplasticGlycolysisHexokinaseHumansLiver NeoplasmsReceptors, AndrogenSignal TransductionUp-RegulationAR protein, humanCREB1 protein, humanCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinHexokinaseHK2 protein, humanReceptors, AndrogenAndrogen receptorCREBGlycolysisHexokinase 2Liver cancerMetabolism

Identifiers

What OpenQuestion 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 OpenQuestion graph.