ArticleOncotarget2016
Stimulation of prolactin receptor induces STAT-5 phosphorylation and cellular invasion in glioblastoma multiforme.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Prolactin as a Candidate Biomarker in Non-Small Cell Lung Cancer: Implications for Personalized Medicine and Post-Treatment Risk Stratification.Journal of personalized medicine · 2026Review
- Prolactin Drives Iron Release from Macrophages and Uptake in Mammary Cancer Cells through CD44.International journal of molecular sciences · 2024Article
- The brain as a source and a target of prolactin in mammals.Neural regeneration research · 2022Review
- Connections between prolactin and ovarian cancer.PloS one · 2021Article
- Human Cytomegalovirus Infection Induces High Expression of Prolactin and Prolactin Receptors in Ovarian Cancer.Biology · 2020Article
- Prolactin and its receptor as therapeutic targets in glioblastoma multiforme.Scientific reports · 2019Article
- Article
- An in vivo half-life extended prolactin receptor antagonist can prevent STAT5 phosphorylation.PloS one · 2019Article
- Article
- Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide.Nucleic acids research · 2018Article
- Glioblastoma research: US and international networking achievements.Oncotarget · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor in humans and is characterized with poor outcome. In this study, we investigated components of prolactin (Prl) system in cell models of GBM and in histological tissue sections obtained from GBM patients. Expression of Prolactin receptor (PrlR) was detected at high levels in U251-MG, at low levels in U87-MG and barely detectable in U373 cell lines and in 66% of brain tumor tissues from 32 GBM patients by immunohistochemical technique. In addition, stimulation of U251-MG and U87-MG cells but not U373 with Prl resulted in increased STAT5 phosphorylation and only in U251-MG cells with increased cellular invasion. Furthermore, STAT5 phosphorylation and cellular invasion induced in Prl stimulated cells were significantly reduced by using a Prl receptor antagonist that consists of Prl with four amino acid replacements. We conclude that Prl receptor is expressed at different levels in the majority of GBM tumors and that blocking of PrlR in U251-MG cells significantly reduce cellular invasion.
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What OpenQuestion holds
Registered trials
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.