Evidence map›Paper›PMID 27867534›Full record

ArticleCell discovery2016

NANOG reprograms prostate cancer cells to castration resistance via dynamically repressing and engaging the AR/FOXA1 signaling axis.

Collene R Jeter, Bigang Liu, Yue Lu, Hsueh-Ping Chao, Dingxiao Zhang, Xin Liu, Xin Chen, Qiuhui Li, Kiera Rycaj, Tammy Calhoun-Davis and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.6field-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

44 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. KInternational journal of molecular sciences · 2021
    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

16 authors at 2 institutions in 1 country.

Collene R JeterDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Bigang LiuDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Yue LuDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Hsueh-Ping ChaoDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Dingxiao ZhangDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Xin LiuDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Xin ChenDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Qiuhui LiDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Kiera RycajDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA.
Tammy Calhoun-DavisDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Li YanDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute , Buffalo, NY, USA.
Qiang HuDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute , Buffalo, NY, USA.
Jianmin WangDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute , Buffalo, NY, USA.
Jianjun ShenDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center , Smithville, TX, USA.
Song LiuDepartment of Biostatistics and Bioinformatics, Roswell Park Cancer Institute , Buffalo, NY, USA.
Dean G TangDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA; Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY, USA; Cancer Stem Cell Institute, Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine, Shanghai, China; Centers for Cancer Epigenetics, Stem Cell and Developmental Biology, RNA Interference and Non-coding RNAs and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · USRoswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
Decoding NanogP8 in TumorigenesisR01CA155693 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI TANG, DEAN G. · 2012 to 2016
$1.6M
NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA155693
6 · The paper itself

Abstract

The pluripotency transcription factor NANOG has been implicated in tumor development, and NANOG-expressing cancer cells manifest stem cell properties that sustain tumor homeostasis, mediate therapy resistance and fuel tumor progression. However, how NANOG converges on somatic circuitry to trigger oncogenic reprogramming remains obscure. We previously reported that inducible NANOG expression propels the emergence of aggressive castration-resistant prostate cancer phenotypes. Here we first show that endogenous NANOG is required for the growth of castration-resistant prostate cancer xenografts. Genome-wide chromatin immunoprecipitation sequencing coupled with biochemical assays unexpectedly reveals that NANOG co-occupies a distinctive proportion of androgen receptor/Forkhead box A1 genomic loci and physically interacts with androgen receptor and Forkhead box A1. Integrative analysis of chromatin immunoprecipitation sequencing and time-resolved RNA sequencing demonstrates that NANOG dynamically alters androgen receptor/Forkhead box A1 signaling leading to both repression of androgen receptor-regulated pro-differentiation genes and induction of genes associated with cell cycle, stem cells, cell motility and castration resistance. Our studies reveal global molecular mechanisms whereby NANOG reprograms prostate cancer cells to a clinically relevant castration-resistant stem cell-like state driven by distinct NANOG-regulated gene clusters that correlate with patient survival. Thus, reprogramming factors such as NANOG may converge on and alter lineage-specific master transcription factors broadly in somatic cancers, thereby facilitating malignant disease progression and providing a novel route for therapeutic resistance.

Indexed as

ARcancer stem cellscastration resistanceFOXA1NANOGprostate cancer

Identifiers

PMID27867534
PMCPMC5109294
OpenAlexW2554826323

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.