Τόμος 35 (2021) – Τεύχος 3 –Άρθρο 6 – Review of Clinical Pharmacology and Pharmacokinetics – Διεθνής Έκδοση – Volume 35 (2021) – Issue 3 – Article 6 – Review of Clinical Pharmacology and Pharmacokinetics – International Edition

Open Access-Title

The role of Notch 2 in primary human breast epithelial cells: a preliminary ex vivo study

Author

Alexios- Fotios A. Mentis, Panagiotis Tsikouras, Panagiotis Peitsidis, Stefanos Zervoudis

University Research Institute of Maternal and Child Health and Precision Medicine, UNESCO Chair on Adolescent Health Care, National and Kapodistrian University of Athens (NKUA), GR-11527 Athens, Greece
Department of Obstetrics and Gynecology, Democritus University of Thrace, Alexandroupolis, Greece
Rea Hospital, Breast Clinic & Greek-French Breast Unit, Athens, Greece

Citation

A-F. A. Mentis, P. Tsikouras, P. Peitsidis, S. Zervoudis. The role of Notch 2 in primary human breast epithelial cells: a preliminary ex vivo study. Review Clin. Pharmacol. Pharmacokinet. 2021, 35, 3, 123-134. DOI: 10.5281/zenodo.10048439

Publication Date
Republication Date
15-12-2021
27-10-2021
Full Text Language

English

DOI: 10.5281/zenodo.10048439

Keywords
Breast cancer; Notch receptor; molecular biology; oncology; metastasis; extracellular matrix
Other Terms

Original Study

Summary
Breast cancer represents a major form of cancer affecting around one out of eight women in resource-rich countries. A hallmark of cancer, including breast cancer, is the dysregulation of intracellular signalling, a notably example of which is the family of Notch (Notch 1 to 4) receptor. While the effects of Notch 1 intracellular signalling have been significantly studied in breast cancer, those of Notch 2, −which shares 37% similarity to Notch1 receptor−, remain far from completely understood. Here, we studied Notch 2 intracellular signalling in human primary breast epithelial cells. Our results showed that: a) Notch 2 signalling may activate different transcription factors than Notch 1 signalling does, b), Notch 2 signalling causes downregulation of ΔΝp63 expression levels, and c) Notch 2 signalling causes distinct changes in the expression levels of integrin proteins in our samples examined. Therefore, if the differences in Notch 1 and Notch2 result in distinct genetic or phenotypic signatures, −an issue to be verified in future studies−, it could be anticipated that targeting Notch 1 and Notch 2 with specific antibodies might lead to distinct therapeutic approaches. 
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