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Expression Profiles of Dopamine-Related Genes and miRNAs Regulating Their Expression in Breast Cancer

Authors :
Tomasz Sirek
Agata Sirek
Przemysław Borawski
Izabella Ryguła
Katarzyna Król-Jatręga
Marcin Opławski
Dariusz Boroń
Michał Chalcarz
Piotr Ossowski
Konrad Dziobek
Nikola Zmarzły
Kacper Boroń
Patrycja Mickiewicz
Beniamin Oskar Grabarek
Source :
International Journal of Molecular Sciences, Vol 25, Iss 12, p 6546 (2024)
Publication Year :
2024
Publisher :
MDPI AG, 2024.

Abstract

This study aimed to assess the expression profile of messenger RNA (mRNA) and microRNA (miRNA) related to the dopaminergic system in five types of breast cancer in Polish women. Patients with five breast cancer subtypes were included in the study: luminal A (n = 130), luminal B (n = 196, including HER2−, n = 100; HER2+, n = 96), HER2+ (n = 36), and TNBC (n = 43); they underwent surgery, during which tumor tissue was removed along with a margin of healthy tissue (control material). The molecular analysis included a microarray profile of mRNAs and miRNAs associated with the dopaminergic system, a real-time polymerase chain reaction preceded by reverse transcription for selected genes, and determinations of their concentration using enzyme-linked immunosorbent assay (ELISA). The conducted statistical analysis showed that five mRNAs statistically significantly differentiated breast cancer sections regardless of subtype compared to control samples; these were dopamine receptor 2 (DRD2), dopamine receptor 3 (DRD3), dopamine receptor 25 (DRD5), transforming growth factor beta 2 (TGF-β-2), and caveolin 2 (CAV2). The predicted analysis showed that hsa-miR-141-3p can regulate the expression of DRD2 and TGF-β-2, whereas hsa-miR-4441 is potentially engaged in the expression regulation of DRD3 and DRD5. In addition, the expression pattern of DRD5 mRNA can also be regulated by has-miR-16-5p. The overexpression of DRD2 and DRD3, with concomitant silencing of DRD5 expression, confirms the presence of dopaminergic abnormalities in breast cancer patients. Moreover, these abnormalities may be the result of miR-141-3P, miR-16-5p, and miR-4441 activity, regulating proliferation or metastasis.

Details

Language :
English
ISSN :
14220067 and 16616596
Volume :
25
Issue :
12
Database :
Directory of Open Access Journals
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
edsdoj.6c5b16638f0b4694b8c33bcbc52b69a2
Document Type :
article
Full Text :
https://doi.org/10.3390/ijms25126546