Date of Presentation
7-29-2026 2:00 PM
College
College of Science & Mathematics
Faculty Sponsor(s)
Dr. Alpaugh
Poster Abstract
Oncogenic E-cadherin-dependent metastasis is a paradoxical mechanism of cancer progression whereby E-cadherin, a cell-to-cell adhesion protein that normally suppresses tumor invasion, instead promotes the formation of cohesive cell tumor clusters that collectively invade surrounding tissues and metastasize. This phenomenon has been extensively studied using inflammatory breast cancer (IBC) models, including the MARY-X xenograft and SUM149 cell line, while comparisons with other breast cancer models such as MDA-MB-231 continue to provide insight into E-cadherin-independent metastatic mechanisms. This project reviews recent literature investigating the molecular mechanisms behind it and evaluates emerging therapeutic strategies targeting E-cadherin-associated cellular pathways. Laboratory techniques, including spheroid generation through agarose plate preparation and use of extracellular matrices to produce biomimetics of metastasis are presented to illustrate experimental approaches used to investigate E-cadherin-dependent metastatic processes in vitro. Continued research into E-cadherin-mediated signaling and targeted therapeutic interventions may improve our understanding of cancer and contribute to the development of more effective treatments for aggressive breast cancers.
Student Keywords
Oncogenic E-cadherin-Dependent Metastasis, Potential Therapeutic Interventions
Disciplines
Biology
Document Type
Poster
Included in
Oncogenic E-cadherin-Dependent Metastasis and Potential Therapeutic Interventions
Oncogenic E-cadherin-dependent metastasis is a paradoxical mechanism of cancer progression whereby E-cadherin, a cell-to-cell adhesion protein that normally suppresses tumor invasion, instead promotes the formation of cohesive cell tumor clusters that collectively invade surrounding tissues and metastasize. This phenomenon has been extensively studied using inflammatory breast cancer (IBC) models, including the MARY-X xenograft and SUM149 cell line, while comparisons with other breast cancer models such as MDA-MB-231 continue to provide insight into E-cadherin-independent metastatic mechanisms. This project reviews recent literature investigating the molecular mechanisms behind it and evaluates emerging therapeutic strategies targeting E-cadherin-associated cellular pathways. Laboratory techniques, including spheroid generation through agarose plate preparation and use of extracellular matrices to produce biomimetics of metastasis are presented to illustrate experimental approaches used to investigate E-cadherin-dependent metastatic processes in vitro. Continued research into E-cadherin-mediated signaling and targeted therapeutic interventions may improve our understanding of cancer and contribute to the development of more effective treatments for aggressive breast cancers.