Date of Award
2011
Degree Type
Thesis
Degree Name
Master of Science
Program
Anatomy and Cell Biology
Supervisor
Dr. Peeyush Lala
Abstract
Although the molecular mechanisms underlying lymphangiogenesis associated with breast cancer continue to remain insufficiently understood, a growing body of evidence suggests that many of the currently unknown answers revolve around the crosstalk between the lymphangiogenic factor VEGF-C and chemokines. The present study proposed the CCL21/CCR7 chemokine axis as a regulatory mechanism of VEGF-C mediated breast cancer-induced lymphangiogenesis. In order to address the hypothesis, the positive correlations between CCR7 signalling and VEGF-C expression/secretion by MDA-MB-231 cells were sought, along with the molecular mechanism underlying their correlation. Furthermore, the direct effect of CCL21/CCR7 interaction on lymphatic endothelial cells (LECs) was tested through a series of in vitro lymphangiogenic assays. CCL21/CCR7 axis has been found to regulate lymphangiogenesis in two distinct ways: i) directly, through stimulation of the lymphangiogenic traits of LECs; and ii) indirectly, through the promotion of VEGF-C secretion by breast cancer cells. These results suggest a novel role of the CCL21/CCR7 axis in the promotion of breast cancer-induced lymphangiogenesis.
Recommended Citation
Tutunea-Fatan, Elena, "THE ROLE OF CCL21/CCR7 CHEMOKINE AXIS IN VEGF-C MEDIATED BREAST CANCER INDUCED LYMPHANGIOGENESIS" (2011). Digitized Theses. 3571.
https://ir.lib.uwo.ca/digitizedtheses/3571