ArticleCell death & disease2019
Bromocriptine and cabergoline induce cell death in prolactinoma cells via the ERK/EGR1 and AKT/mTOR pathway respectively.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- The Role of Activation of PI3K/AKT/mTOR and RAF/MEK/ERK Pathways in Aggressive Pituitary Adenomas-New Potential Therapeutic Approach-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- circOMA1 delivered by exosomes regulates DRD2‑mediated prolactinoma resistance.International journal of molecular medicine · 2026Article
- Dopamine agonist-associated fibrosis in prolactinomas: clinical challenges, impacts on the tumor microenvironment, and future directions.Frontiers in endocrinology · 2026Review
- Spatial transcriptomics reveal PI3K-AKT and metabolic alterations in aggressive, treatment-resistant lactotroph pituitary neuroendocrine tumors.Acta neuropathologica communications · 2025Article
- Bromocriptine sensitivity in bromocriptine-induced drug-resistant prolactinomas is restored by inhibiting FGF19/FGFR4/PRL.Journal of endocrinological investigation · 2025Article
- Anti-hypertensive effect and potential mechanism of gastrodia-uncaria granules based on network pharmacology and experimental validation.Journal of clinical hypertension (Greenwich, Conn.) · 2024Article
- Bone Morphogenetic Protein Signaling Agonist SB4 (BMPSB4) Inhibits Corticotroph Pituitary Neuroendocrine Tumors by Activation of Autophagy via a BMP4/SMADs-Dependent Pathway.ACS pharmacology & translational science · 2024Article
- Sini San ameliorates lipid metabolism in hyperprolactinemia rat with liver-depression.Current research in food science · 2024Article
- A study on the correlations of PRL levels with anxiety, depression, sleep, and self-efficacy in patients with prolactinoma.Frontiers in endocrinology · 2024Article
- Oxidative stress in pituitary neuroendocrine tumors: Affecting the tumor microenvironment and becoming a new target for pituitary neuroendocrine tumor therapy.CNS neuroscience & therapeutics · 2023Review
- MicroRNA-137 inhibits pituitary prolactinoma proliferation by targeting AKT2.Journal of endocrinological investigation · 2023Article
- Intranasal 15d-PGJ2 inhibits the growth of rat lactotroph pituitary neuroendocrine tumors by inducing PPARγ-dependent apoptotic and autophagic cell death.Frontiers in neuroscience · 2023Article
- Sensor technologies for quality control in engineered tissue manufacturing.Biofabrication · 2022Review
- The dopaminergic control of Cushing's syndrome.Journal of endocrinological investigation · 2022Review
- Recent Advances in Treatment of Recurrent Spontaneous Abortion.Obstetrical & gynecological survey · 2022Review
- Current and Emerging Medical Therapies in Pituitary Tumors.Journal of clinical medicine · 2022Review
- Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022Review
- Prediction and Identification of GPCRs Targeting for Drug Repurposing in Osteosarcoma.Frontiers in oncology · 2022Article
- Curcumin Sensitizes Prolactinoma Cells to Bromocriptine by Activating the ERK/EGR1 and Inhibiting the AKT/GSK-3β Signaling Pathway In Vitro and In Vivo.Molecular neurobiology · 2021Article
- Pituitary Adenomas: From Diagnosis to Therapeutics.Biomedicines · 2021Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The treatment of hyperprolactinemia is based on the use of dopamine agonists, mainly bromocriptine (BRC) and cabergoline (CAB). They reduce tumour size effectively and restore gonadal function. However, there is a difference in drug sensitivity between CAB and BRC in patients with prolactinoma, although the underlying mechanisms are still unknown. Thus, we investigated whether there are differences in tumour sensitivity to CAB and BRC and their possible differential mechanisms in two prolactinoma cell lines. In our study, we found that GH3 cells are more sensitive to BRC and that MMQ cells are more sensitive to CAB. Moreover, BRC and CAB elicited cell death via different pathways; BRC induced prolactinoma cell death mainly through the apoptosis pathway, and CAB induced pituitary prolactinoma cell death mainly via the autophagic cell death pathway. Using gene microarray analysis, we found that BRC induces the apoptosis of prolactinoma cells through the ERK/EGR1 signalling pathway, whereas CAB induces autophagic death by inhibiting the AKT/mTOR signalling pathway. Our study showed the difference in tumour sensitivity and differential mechanisms in BRC- and CAB-treated prolactinoma cells, which provides a theoretical basis for the accurate treatment of prolactinoma.
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