ReviewCancers2021
Crosstalk between PRLR and EGFR/HER2 Signaling Pathways in Breast Cancer.
Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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.
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.
Who cites it
45 citing papers in PubMed, 86 citations in OpenAlex.
- Beyond lactation: Central oxytocin in maternal mental health and disease.Neuroscience and biobehavioral reviews · 2026Review
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- HER2-targeted doxorubicin-loaded cell-derived extracellular vesicles induce apoptosis of breast cancer cells via ROS/TXNIP pathway activation.Cancer cell international · 2026Article
- Impact of immune microenvironment on immune checkpoint inhibitor response in HER2-overexpressing urothelial carcinoma.Discover oncology · 2026Article
- Bispecific antibody-drug conjugates: a modular blueprint for next-generation cancer therapeutics.Archives of pharmacal research · 2026Review
- Gene Expression Profiling to Unveil Novel Biomarkers for Early Diagnosis and Therapies for Breast Cancer.Current topics in medicinal chemistry · 2026Article
- Unraveling the Carcinogenic Mechanisms of Food Contaminants: An Integrated in Silico Framework Combining Network Toxicology, Machine Learning, and Molecular Docking.Journal of food science · 2025Article
- Review
- Article
- Article
- Clustering of Membrane Receptors: Insights from DNA Origami-Based Approaches.Small (Weinheim an der Bergstrasse, Germany) · 2025Review
- Resistant PRL-secreting PitNET associated with breast carcinoma: a case report and literature review.International cancer conference journal · 2025Article
- Exploring the Genetic Orchestra of Cancer: The Interplay Between Oncogenes and Tumor-Suppressor Genes.Cancers · 2025Review
- CouldBiomedicines · 2025Article
- Association of Selected STAT Inhibitors with Prolactin-Induced Protein (PIP) in Breast Cancer.International journal of molecular sciences · 2025Article
- GPNMB is a novel binding partner of FGFR1 that affects tumorigenic potential through AKT phosphorylation in TNBC.Cancer science · 2025Article
- An investigation of the pattern and mechanism of comorbidity in patients with Hashimoto's thyroiditis.Frontiers in endocrinology · 2025Article
- Polyphenols as Immunomodulators and Epigenetic Modulators: An Analysis of Their Role in the Treatment and Prevention of Breast Cancer.Nutrients · 2024Review
- Oncogenic RTKs sensitize cancer cells to ferroptosis via c-Myc mediated upregulation of ACSL4.Cell death & disease · 2024Article
- Crystal structure and Hirshfeld surface analysis of (Acta crystallographica. Section E, Crystallographic communications · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Prolactin receptor (PRLR) and epidermal growth factor receptor (EGFR/ERBB) signaling pathways activated by prolactin (PRL) and epidermal growth factor (EGF), have a major role in the mammary gland development and in the etiology of breast cancer, respectively. ER+ breast tumors comprise up to 75% of all breast cancers and 10% of these are HER2+. Elevated levels of PRLR in breast tumors, high circulating levels of PRL and increased expression of ERBB1/2 in patients that become resistant to endocrine therapy have shown to be associated with higher risk of cancer progression. In this review, we examine the role of crosstalk between PRLR and ERBB1/2 signaling pathways in the activation of unliganded ERα, cyclin-D1 and other oncogenic factors (MYC, FOS, JUN) in breast cancer. PRL/PRLR and EGF/EGFR induces phosphorylation of ERα through activation of MEK/MAPK and PI3K/AKT signaling pathways. PRL in breast cancer cells via PRLR/JAK2 can also induce phosphorylation of ERBB2/HER2, which in turn activates the downstream RAS/MEK/ERK pathway required for ERα phosphorylation. EGFR, independent of PRL/PRLR, can activate STAT5 indirectly via c-SRC and drive the expression of target genes involved in cell proliferation and survival. The crosstalk between PRLR and HER2, where PRL induces HER2 signaling can be an alternative route for ERα activation to induce transcription of PRLR and other ER target genes. We believe that overexpression of EGFR/HER2 and PRLR in breast tumors could maximize the actions of their ligands, and further induce cell proliferation promoting malignancy. This could also explain the resistance to endocrine therapy resulting in tumor growth.
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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.