Is prolactin receptor signaling a target in dopamine-resistant prolactinomas?

Ferraris, Jimena

doi:10.3389/fendo.2022.1057749

Cited by 2 publications

(1 citation statement)

References 79 publications

(141 reference statements)

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“…AKT1, as a member of AKT kinase, takes part in cellular progress, namely cell proliferation, apoptosis, and glucose metabolism. The PI3K/AKT pathway has formerly been reported to be connected with prolactinoma development (Dworakowska et al, 2009; Ferraris, 2022). It was shown that the PVE markedly suppressed the expression of AKT1 and Bcl-2/BAX protein.…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology to Explore the Mechanism of Prunella vulgaris L. Against Prolactinoma

Meng,

Ni,

Cao

et al. 2023

Pharmacognosy Magazine

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Objectives Prolactinoma is a common intracranial tumor with a high incidence and serious harm to human health. At present, there is only one therapeutic drug in China, bromocriptine, and the Chinese herb Prunella vulgaris L.( P. vulgaris)(PV) has shown certain anti-prolactinoma effects in the early stage. We expect to develop a candidate drug against prolactinoma. Materials and Methods First, the extracts of P. vulgaris L.(PVE)were extracted with water, and the cell proliferation test of rat pituitary tumor cells MMQ was checked by the Cell Counting Kit-8 (CCK-8) assay. Then, core targets and correlative pathways were selected by the “protein–protein interaction” (PPI) network and the “PV–Target–Prolactinoma” network. The core targets and main components simulate the binding by molecular docking. Finally, the PVE and MMQ cells were used to verify the results. Results Through the CCK-8 assay, the PVE inhibited the proliferation of MMQ cells. From the network pharmacology, the 21 targets, 9 signaling pathways, and 20 gene ontology (GO) projects were attained ( p < .05). As a result the estrogen receptor α (ESR1), RAC-alpha serine/threonine-protein kinase(AKT1), and mitogen-activated protein kinase 3(MAPK3)were the core targets of protein against prolactinomas, which was in line with western blotting analysis. Conclusion Our findings demonstrate that the PVE was verified against prolactinomas through the ESR1, MAPK3 targets, and the phosphoinositide 3-kinase/protein kinase B pathway.

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Section: Discussionmentioning

confidence: 99%

Network Pharmacology to Explore the Mechanism of Prunella vulgaris L. Against Prolactinoma

Meng,

Ni,

Cao

et al. 2023

Pharmacognosy Magazine

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Resistance to dopamine agonists in the treatment of prolactinomas: diagnostic criteria, mechanisms and ways to overcome it

Ilovayskaya,

Vagapova

2024

Almanac of Clinical Medicine

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The priority treatment approach for prolactinomas is therapy with dopamine agonists, which allows for elimination of clinical symptoms, normalization of prolactin levels, reduction of the adenoma size and prevention of metabolic abnormalities in the majority of patients. Nevertheless, 10 to 20% of patients are resistant to dopamine agonists. The aim of this review is to analyze literature data on the source mechanisms and potential ways to overcome the resistance of prolactinomas to dopamine agonists. The criteria of a prolactinoma's resistance to dopamine agonists are as follows: 1) no normalization of serum prolactin levels and/or 2) no reduction of the adenoma volume by at least 50% after treatment of bromocriptine at a dose of ≤ 15 mg/day or cabergoline at a dose of ≤ 3 mg/week for at least 6 months. Full resistance is characterized by both no biochemical and no anti-tumor effects, whereas in partial resistance, prolactin levels can be decreased but not normalized, or the adenoma size can be reduced by less than 50% of the initial. The clinical and morphological predictors of prolactinoma resistance to dopamine agonists are male gender, young age, big size of the adenoma and its invasion into the sinus cavernosus, hypointensive and/or heterogeneous MRI signal on Т2 weighed images, and cystic components within the tumor. The main molecular genetic markers are: decreased expression of dopamine and estrogen receptors, higher proliferation index Ki-67 ≤ 3%, as well as the MENIN, AIP, SF3B1, PRDM2 gene mutations. In case of resistance to bromocriptine, it is recommended to switch the patient to cabergoline. In partial resistance to standard doses of cabergoline, it is possible to increase the dose up to a maximally tolerated. Neurosurgery and/or radiation surgery is recommended in cases of full resistance to dopamine agonists or an aggressive tumor. For very aggressive/malignant tumors, or in the event of their extended growth after surgery, temozolomide is recommended as adjuvant therapy.

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Is prolactin receptor signaling a target in dopamine-resistant prolactinomas?

Cited by 2 publications

References 79 publications

Network Pharmacology to Explore the Mechanism of Prunella vulgaris L. Against Prolactinoma

Network Pharmacology to Explore the Mechanism of Prunella vulgaris L. Against Prolactinoma

Resistance to dopamine agonists in the treatment of prolactinomas: diagnostic criteria, mechanisms and ways to overcome it

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