Evidence map›Paper›PMID 31312936›Full record

ArticleInvestigational new drugs2020

Stimulation of neuroendocrine differentiation in prostate cancer cells by GHRH and its blockade by GHRH antagonists.

Laura Muñoz-Moreno, María J Carmena, Andrew V Schally, Juan C Prieto, Ana M Bajo

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. GHRH and the prostate.Reviews in endocrine & metabolic disorders · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Advances in neuroendocrine prostate cancer research: From model construction to molecular network analyses.Laboratory investigation; a journal of technical methods and pathology · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. P53 versus inflammation: an update.Cell cycle (Georgetown, Tex.) · 2020
    Review
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

5 authors at 2 institutions in 2 countries.

Laura Muñoz-MorenoDepartment of Systems Biology, University of Alcalá, 28871, Alcalá de Henares, Spain.
María J CarmenaDepartment of Systems Biology, University of Alcalá, 28871, Alcalá de Henares, Spain.
Andrew V SchallyVeterans Affairs Medical Center, Endocrine, Polypeptide and Cancer Institute, Miami, FL, 33125, USA.
Juan C PrietoDepartment of Systems Biology, University of Alcalá, 28871, Alcalá de Henares, Spain.
Ana M BajoDepartment of Systems Biology, University of Alcalá, 28871, Alcalá de Henares, Spain. ana.bajo@uah.es.ORCID 0000-0002-4944-4222
Universidad de Alcalá · ESUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is the second leading cause of cancer-related deaths among men in developed countries. Neuroendocrine prostate cancer, in particular, is associated with an aggressive phenotype and a poor prognosis. Neuroendocrine cells produce and secrete peptide hormones and growth factors in a paracrine/autocrine manner which promote the progression of the disease. Recent studies have demonstrated that extracellular vesicles or exosomes are released by prostate cancer cells, supporting the spread of prostate cancer. Hence, the aim of this study was to investigate the effect of growth hormone-releasing hormone (GHRH) on neuroendocrine differentiation (NED) in the androgen-dependent prostate cancer cell line LNCaP and the molecular mechanisms underlying these effects. GHRH induced an increase in the percentage of neurite-bearing cells and in the protein levels of Neuron-Specific Enolase. Both effects were blocked by the GHRH receptor antagonist MIA-690. In addition, pretreatment of these cells with the calcium chelator BAPTA, the EGFR inhibitor AG-1478 or the HER2 inhibitor AG-825 reduced the effect of GHRH, suggesting that the GHRH-induced stimulation of NED involves calcium channel activation and EGFR/HER2 transactivation. Finally, PC3-derived exosomes led to an increase in NED, cell proliferation and cell adhesion. Altogether, these findings suggest that GHRH antagonists should be considered for in the management of neuroendocrine prostate cancer.

Indexed as

AndrogensCell AdhesionCell DifferentiationCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesGrowth Hormone-Releasing HormoneHumansMaleNeuroendocrine CellsPC-3 CellsProstatic NeoplasmsQuinazolinesTyrphostinsAndrogensErb-b2 Receptor Tyrosine KinasesGrowth Hormone-Releasing HormoneQuinazolinesRTKI cpdTyrphostinsExosomesGHRHLNCaP cellsNeuroendocrine differentiationPC3 cellsProstate cancer

Identifiers

PMID31312936
OpenAlexW2958348195

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.