Evidence map›Paper›PMID 23851444›Full record

ArticleMolecular cancer research : MCR2013

Angiogenin mediates androgen-stimulated prostate cancer growth and enables castration resistance.

Shuping Li, Miaofen G Hu, Yeqing Sun, Norie Yoshioka, Soichiro Ibaragi, Jinghao Sheng, Guangjie Sun, Koji Kishimoto, Guo-Fu Hu

Open access · hybridAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

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  13. Review
  14. Three decades of research on angiogenin: a review and perspective.Acta biochimica et biophysica Sinica · 2016
    Review
  15. Article
  16. Article
  17. Mechanism and Function of Angiogenin in Prostate Cancer.Zhongguo sheng wu hua xue yu fen zi sheng wu xue bao = Chinese journal of biochemistry and molecular biology · 2015
    Article
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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

9 authors at 4 institutions in 3 countries.

Shuping LiMolecular Oncology Research Institute, Tufts Medical Center, 800 Washington Street, Boston, MA 02111. ghu@tuftsmedicalcenter.org.
Miaofen G Hu
Yeqing Sun
Norie Yoshioka
Soichiro Ibaragi
Jinghao Sheng
Guangjie Sun
Koji Kishimoto
Guo-Fu Hu
Okayama University · JPMassachusetts General Hospital · USTufts Medical Center · USDalian Maritime University · CN

Funding

The mechanism of angiogenin-induced angiogenesisR01CA105241 · NCI · TUFTS MEDICAL CENTER · PI HU, GUO-FU · 2005 to 2015
$2.8M
NCI NIH HHS R01 CA105241
6 · The paper itself

Abstract

unlabelledThe androgen receptor (AR) is a critical effector of prostate cancer development and progression. Androgen-dependent prostate cancer is reliant on the function of AR for growth and progression. Most castration-resistant prostate cancer (CRPC) remains dependent on AR signaling for survival and growth. Ribosomal RNA (rRNA) is essential for both androgen-dependent and castration-resistant growth of prostate cancer cells. During androgen-dependent growth of prostate cells, androgen-AR signaling leads to the accumulation of rRNA. However, the mechanism by which AR regulates rRNA transcription is unknown. Here, investigation revealed that angiogenin (ANG), a member of the secreted ribonuclease superfamily, is upregulated in prostate cancer and mediates androgen-stimulated rRNA transcription in prostate cancer cells. Upon androgen stimulation, ANG undergoes nuclear translocation in androgen-dependent prostate cancer cells, where it binds to the rDNA promoter and stimulates rRNA transcription. ANG antagonists inhibit androgen-induced rRNA transcription and cell proliferation in androgen-dependent prostate cancer cells. Interestingly, ANG also mediates androgen-independent rRNA transcription through a mechanism that involves its constitutive nuclear translocation in androgen-insensitive prostate cancer cells, resulting in a constant rRNA overproduction and thereby stimulating cell proliferation. Critically, ANG overexpression in androgen-dependent prostate cancer cells enables castration-resistant growth of otherwise androgen-dependent cells. Thus, ANG-stimulated rRNA transcription is not only an essential component for androgen-dependent growth of prostate cancer but also contributes to the transition of prostate cancer from androgen-dependent to castration-resistant growth status. IMPLICATIONS: The ability of angiogenin to regulate rRNA transcription and prostate cancer growth makes it a viable target for therapy.

Indexed as

AndrogensAngiogenesis Inducing AgentsAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMaleMiceMice, SCIDNeoplasm TransplantationPromoter Regions, GeneticProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantAndrogensAngiogenesis Inducing AgentsangiogeninReceptors, AndrogenRibonuclease, PancreaticRNA, Ribosomal

Identifiers

PMID23851444
PMCPMC3800479
OpenAlexW2096096265

What OpenQuestion holds

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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.