Evidence map›Paper›PMID 28220803›Full record

ArticleProstate cancer and prostatic diseases2017

TCF7 is suppressed by the androgen receptor via microRNA-1-mediated downregulation and is involved in the development of resistance to androgen deprivation in prostate cancer.

M K Siu, W-Y Chen, H-Y Tsai, H-Y Chen, J J Yin, C-L Chen, Y-C Tsai, Y-N Liu

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Article in Prostate cancer and prostatic diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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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

16 citing papers in PubMed, 42 citations in OpenAlex.

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  9. Review
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  12. Oncogenic and tumor-suppressive microRNAs in prostate cancer.Current opinion in endocrine and metabolic research · 2020
    Article
  13. Article
  14. Androgen-Regulated microRNAs (AndroMiRs) as Novel Players in Adipogenesis.International journal of molecular sciences · 2019
    Review
  15. Clinical Significance of Transcription Factor 7 (TCF7) as a Prognostic Factor in Gastric Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  16. Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

M K SiuPhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan.
W-Y ChenDepartment of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
H-Y TsaiGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
H-Y ChenInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
J J YinCell and Cancer Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
C-L ChenDepartment of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Y-C TsaiPhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan.
Y-N LiuPhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan.
Taipei Medical University · TWWan Fang Hospital · TWAcademia Sinica · TWInstitute of Statistical Science, Academia Sinica · TWNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundResistance to androgen deprivation therapy (ADT) represents a key step in the malignant progression of prostate cancer, and mutation to androgen receptor (AR) is one major driver to an androgen-independent phenotype. However, alternative oncogenic pathways that bypass AR signaling have emerged as an important mechanism promoting resistance to ADT. It is known that AR activation can prevent the interaction between β-catenin and T cell factor/lymphoid enhancer-binding factor (TCF/LEF) family, inhibiting the Wnt signaling pathway. The aim of this study was to determine the role of transcription factor 7 (TCF7), a transcription factor best known as a Wnt effector that forms a complex with β-catenin, in the development of advanced prostate cancer. We further investigated the molecular mechanisms by which TCF7 is induced when AR signaling is inactivated.

methodsA novel AR signaling pathway that induces microRNA-1 (miR-1) to suppress metastatic prostate cancer was recently demonstrated (AR-miR-1 signaling axis), and its regulation of Wnt signaling was explored in the current study. Clinical data sets were analyzed for potential targets of AR-miR-1 signaling in the TCF/LEF family, and tissue samples were utilized to validate the relationship. The molecular mechanism and biological functions were demonstrated in prostate cancer cell lines and a mouse xenograft model.

resultsWe demonstrated a molecular mechanism of AR signaling suppressing TCF7 partly through miR-1-mediated downregulation. TCF7 exhibited oncogenic properties and compromised the tumor-suppressive effects of miR-1. Our results also showed that overexpression of TCF7 or disruption of miR-1 function promoted androgen-independent proliferation.

conclusionsWe demonstrated that the AR-miR-1 axis negatively regulates the novel oncogenic factor, TCF7. Dysregulation of TCF7 promoted a survival advantage and resistance to androgen deprivation, suggesting its therapeutic potential for castration-resistant prostate cancer.

Indexed as

AndrogensAnimalsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMaleMiceMicroRNAsNeoplasm MetastasisProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionT Cell Transcription Factor 1Xenograft Model Antitumor AssaysAndrogensMicroRNAsMIRN1 microRNA, humanReceptors, AndrogenT Cell Transcription Factor 1TCF7 protein, human

Identifiers

PMID28220803
OpenAlexW2591470397

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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.