ArticleOncotarget2015
Suppression of mTOR pathway and induction of autophagy-dependent cell death by cabergoline.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03400865 (The Effect of Combined Treatment of Cabergoline With Hydroxychloroquine/Chloroquine for Resistant Prolactinomas), which is not on this map. Cited by 23 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.
The Effect of Combined Treatment of Cabergoline With Hydroxychloroquine/Chloroquine for Resistant Prolactinomas
Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- The Marine-Derived Cyclopentapeptide Turnagainolide B Suppresses Melanoma via Autophagic Flux Disruption and Inhibits Tumorigenesis In Vivo.Marine drugs · 2026Article
- Cabergoline-induced NDFIP1 upregulation in pituitary neuroendocrine tumor cells activates mTOR signaling and contributes to cabergoline resistance.Journal of neuro-oncology · 2025Article
- Targeting Autophagy for Pituitary Tumors.Cancers · 2025Review
- Real-life data on pasireotide in monotherapy or combined in active Cushing's disease.Frontiers in endocrinology · 2025Article
- Pituitary Tumorigenesis-Implications for Management.Medicina (Kaunas, Lithuania) · 2023Review
- The dopaminergic control of Cushing's syndrome.Journal of endocrinological investigation · 2022Review
- Current and Emerging Medical Therapies in Pituitary Tumors.Journal of clinical medicine · 2022Review
- ERK inhibition in glioblastoma is associated with autophagy activation and tumorigenesis suppression.Journal of neuro-oncology · 2022Article
- Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022Review
- Autophagy in normal pituitary and pituitary tumor cells and its potential role in the actions of somatostatin receptor ligands in acromegaly.Reviews in endocrine & metabolic disorders · 2021Review
- Large Scale Molecular Studies of Pituitary Neuroendocrine Tumors: Novel Markers, Mechanisms and Translational Perspectives.Cancers · 2021Review
- Resistance to Dopamine Agonists in Pituitary Tumors: Molecular Mechanisms.Frontiers in endocrinology · 2021Review
- Brusatol Inhibits Tumor Growth and Increases the Efficacy of Cabergoline against Pituitary Adenomas.Oxidative medicine and cellular longevity · 2021Article
- Activation of dopamine receptor D1 inhibits glioblastoma tumorigenicity by regulating autophagic activity.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Effects of octreotide on autophagy markers and cell viability markers related to metabolic activity in rat pituitary tumor cells.Pituitary · 2020Article
- A Novel Mechanism Regulating Dopamine Receptor Type 2 Signal Transduction in Pituitary Tumoral Cells: The Role of cAMP/PKA-Induced Filamin A Phosphorylation.Frontiers in endocrinology · 2020Article
- Metformin inhibits growth and prolactin secretion of pituitary prolactinoma cells and xenografts.Journal of cellular and molecular medicine · 2018Article
- Inhibition of mTORC1 by lncRNA H19 via disrupting 4E-BP1/Raptor interaction in pituitary tumours.Nature communications · 2018Article
- The Mechanism and Pathways of Dopamine and Dopamine Agonists in Prolactinomas.Frontiers in endocrinology · 2018Review
- Activation of DRD5 (dopamine receptor D5) inhibits tumor growth by autophagic cell death.Autophagy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cabergoline (CAB), the first-line drug for treatment of prolactinomas, is effective in suppressing prolactin hypersecretion, reducing tumor size, and restoring gonadal function. However, mechanisms for CAB-mediated tumor shrinkage are largely unknown. Here we report a novel cytotoxic mechanism for CAB. CAB induced formation of autophagosome in rat pituitary tumor MMQ and GH3 cells at the early stage through inhibiting mTOR pathway, resulting in higher conversion rates of LC3-I to LC3-II, GFP-LC3 aggregation, and increased autophagosome formation. Interestingly, CAB treatment augmented lysosome acidification and resulted in impaired proteolytic degradation within autolysosomes. This blocked the autophagic flux, leading to the accumulation of p62 aggregation and undigested autolysosomes. Knockdown of ATG7, ATG5, or Becn1, could significantly rescue the CAB-mediated cell death of MMQ cells (p < 0.05). CAB-induced autophagy and blockade of autophagy flux participated in antitumoral action in vivo. In conclusion, our study provides evidence that CAB concomitantly induces autophagy and inhibits the autophagic flux, leading to autophagy-dependent cell death. These findings elucidate novel mechanisms for CAB action.
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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.