ArticleJournal of endocrinological investigation2010
Does prolactin induce apoptosis? Evidences in a prostate cancer in vitro model.
Article in Journal of endocrinological investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- From pituitary cells to prostate gland in health and disease: direct and indirect endocrine connections.Reviews in endocrine & metabolic disorders · 2025Review
- STAT3 activation is required for the antiapoptotic effects of prolactin in cervical cancer cells.Cancer cell international · 2015Article
- High expression of prolactin receptor is associated with cell survival in cervical cancer cells.Cancer cell international · 2013Article
- Small peptides derived from somatotropin domain-containing proteins inhibit blood and lymphatic endothelial cell proliferation, migration, adhesion and tube formation.The international journal of biochemistry & cell biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProlactin (PRL) regulates prostate growth and differentiation. Some studies have suggested that PRL has a pro-apoptotic effect on a myeloma cell line and in newt spermatogonia. The proliferative effect of PRL on prostate cancer cell lines is, however, a controversial area.
aimOn this account, we evaluated the effects of PRL on the prostate cancer cell lines LNCaP and PC3 apoptosis and proliferation. MATERIALS AND
methodsLNCaP and PC3 cells were exposed to increasing concentrations of PRL for 24, 48, 72 and 96 hours. Staining with propidium iodide (PI) and TUNEL assay followed by flow cytometry were used to detect apoptosis. LNCaP and PC3 proliferation was assessed by optical microscopy counting.
resultsPRL induced a dose-dependent decrease of DNA content and an increase of DNA fragmentation in LNCaP after 96 hours of incubation. These effects were observed with physiological concentrations of PRL and were counteracted by a prolactin receptor antagonist. On the other hand, PRL did not have any effect on DNA content or fragmentation in PC3 cells. No effect of PRL on LNCaP and PC3 proliferation was found.
conclusionsThis study indicates that PRL induces apoptosis in the androgen-responsive cell line LNCaP, whereas no effect was observed in the androgen-insensitive PC3 cell line. These findings suggest that androgen responsiveness may be required for PRL to be effective on prostatic cells.
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