Prolactin is a key mammary gland differentiation factor. However, the contribution of prolactin (PRL) to breast carcinogenesis is less clear. Accumulating evidences indicate that in established breast carcinomas autocrine/paracrine PRL can enhance growth/viability of breast cancer cells. Still, it is not known whether the ascribed pro-oncogenic activity of PRL describes fully the role of PRL in regulating breast carcinogenesis. On the other hand a critical role for Ras-Erk1/2 and TGF-beta (Transforming Growth Factor beta) pathway in breast cancer progression has already been established. Our results indicate that blocking PRL signal leads to activation of Ras-Erk1/2 pathway and TGF-beta pathway, two key pathways contributing to breast cancer metastasis. I showed that modulation of PRL signaling in breast cancer cells alters their morphogenic program. My results highlight a critical role for PRL in regulating epithelial plasticity and implicate PRL as invasive suppressor hormone in breast cancer cells.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.97983 |
Date | January 2005 |
Creators | Nouhi, Zaynab. |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Master of Science (Division of Experimental Medicine.) |
Rights | © Zaynab Nouhi, 2005 |
Relation | alephsysno: 002331591, proquestno: AAIMR24758, Theses scanned by UMI/ProQuest. |
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