Subtype-Independent Dysregulation of the Notch Signaling Pathway and Its miRNA Regulators in Breast Cancer
Mitka-Krysiak E., Król-Jatręga K., Ossowski P., Zmarzły N., Bereza K., Ordon P.
Prospective Study with a reported sample of 130, published in Biomedicines (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Biomedicines (2025)
- Reported sample size
- 130
- Source database
- Europe PMC
- PMID
- 41463075
- PMCID
- PMC12730416
- DOI
- 10.3390/biomedicines13123065
Abstract (original English)
Background/Objectives : The Notch signaling pathway regulates cell fate, proliferation, and differentiation, and its dysregulation has been implicated in various cancers, including breast cancer. MicroRNAs (miRNAs) are critical post-transcriptional regulators that can modulate Notch pathway components. The aim of this study was to identify miRNAs that may potentially regulate the expression of Notch pathway-related genes across five molecular subtypes of breast cancer in Polish women. Methods : Tumor and adjacent normal tissue samples were collected from 405 patients with five breast cancer subtypes: luminal A ( n = 130), HER2-negative luminal B ( n = 100), HER2-positive luminal B ( n = 96), non-luminal HER2-positive ( n = 36), and triple-negative breast cancer ( n = 43). Gene expression was profiled using mRNA microarrays and validated with RT-qPCR and ELISA. Candidate regulatory miRNAs were identified by miRNA microarrays and confirmed using the miRDB database. Results : APH1A , CTBP1 , DTX1 , HEY1 , HEY2 , JAG2 , NOTCH4 , TLE2 , and TLE4 were consistently dysregulated across all breast cancer subtypes. Overexpression of HEY1 and JAG2 may be driven by decreased levels of miR-145, miR-98, and miR-381. Conversely, downregulation of TLE4 may be associated with elevated expression of miR-196a and miR-155. No regulatory miRNAs meeting the selection criteria were identified for APH
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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