scholarly journals Signaling and Antiproliferative Effects of Type I and II Gonadotropin-Releasing Hormone Receptors in Breast Cancer Cells

2004 ◽  
Vol 89 (4) ◽  
pp. 1823-1832 ◽  
Author(s):  
Ann R. Finch ◽  
Lisa Green ◽  
James N. Hislop ◽  
Eamonn Kelly ◽  
Craig A. McArdle
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Hormone Receptors ◽  
Gonadotropin Releasing Hormone ◽  
Type I ◽  
Antiproliferative Effects ◽  
Releasing Hormone

scholarly journals Type I Gonadotropin-Releasing Hormone Receptor Mediates the Antiproliferative Effects of GnRH-II on Prostate Cancer Cells

2009 ◽  
Vol 94 (5) ◽  
pp. 1761-1767 ◽  
Author(s):  
Marina Montagnani Marelli ◽  
Roberta M. Moretti ◽  
Stefania Mai ◽  
Joanna Januszkiewicz-Caulier ◽  
Marcella Motta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Hormone Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Type I ◽  
Prostate Cancer Cells ◽  
Antiproliferative Effects ◽  
Releasing Hormone ◽  
Gonadotropin Releasing Hormone Receptor

scholarly journals Type I Gonadotropin-Releasing Hormone Receptor Mediates the Antiproliferative Effects of GnRH-II on Prostate Cancer Cells

2009 ◽  
Vol 23 (4) ◽  
pp. 584-584
Author(s):  
Marina Montagnani Marelli ◽  
Roberta M. Moretti ◽  
Stefania Mai ◽  
Joanna Januszkiewicz-Caulier ◽  
Marcella Motta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Hormone Receptor ◽  
Gonadotropin Releasing Hormone ◽  
Type I ◽  
Prostate Cancer Cells ◽  
Antiproliferative Effects ◽  
Releasing Hormone ◽  
Gonadotropin Releasing Hormone Receptor

scholarly journals Matrix degradation and cell proliferation are coupled to promote invasion and escape from an engineered human breast microtumor

2021 ◽  
Vol 13 (1) ◽  
pp. 17-29
Author(s):  
Emann M Rabie ◽  
Sherry X Zhang ◽  
Andreas P Kourouklis ◽  
A Nihan Kilinc ◽  
Allison K Simi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Type I ◽  
Matrix Degradation ◽  
Human Breast ◽  
Rate Of Invasion

Abstract Metastasis, the leading cause of mortality in cancer patients, depends upon the ability of cancer cells to invade into the extracellular matrix that surrounds the primary tumor and to escape into the vasculature. To investigate the features of the microenvironment that regulate invasion and escape, we generated solid microtumors of MDA-MB-231 human breast carcinoma cells within gels of type I collagen. The microtumors were formed at defined distances adjacent to an empty cavity, which served as an artificial vessel into which the constituent tumor cells could escape. To define the relative contributions of matrix degradation and cell proliferation on invasion and escape, we used pharmacological approaches to block the activity of matrix metalloproteinases (MMPs) or to arrest the cell cycle. We found that blocking MMP activity prevents both invasion and escape of the breast cancer cells. Surprisingly, blocking proliferation increases the rate of invasion but has no effect on that of escape. We found that arresting the cell cycle increases the expression of MMPs, consistent with the increased rate of invasion. To gain additional insight into the role of cell proliferation in the invasion process, we generated microtumors from cells that express the fluorescent ubiquitination-based cell cycle indicator. We found that the cells that initiate invasions are preferentially quiescent, whereas cell proliferation is associated with the extension of invasions. These data suggest that matrix degradation and cell proliferation are coupled during the invasion and escape of human breast cancer cells and highlight the critical role of matrix proteolysis in governing tumor phenotype.

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