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What is E-cadherin?

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    Posted: Mar 15 2012 at 7:11am

Newswise — LEXINGTON, Ky. (March 14, 2012) — A new study by University of Kentucky researchers provides insight into developing new treatment strategies for basal-like breast cancer, commonly known as triple-negative breast cancer. This cancer is associated with early metastasis and resistance to chemotherapy and occurs at women at a younger age.

Tumor cells can exploit a cellular program that promotes cell migration and reduces adhesion between cells to spread to distant sites in the body. This cellular program, known as the epithelial-mesenchymal transition, requires large-scale cell movement during embryonic development, tissue remodeling and wound healing. Tumor cells take over this developmental program for their cell movement during invasion and metastasis.

In this EMT process, expression of a cell-to-cell adhesion molecule called E-cadherin, which functions as a “molecular glue” that binds cells to one another, needs to be downregulated in order for cells to disassociate from each other and spread throughout the body. A protein called Snail acts as a master switch in the cell's nucleus to suppress E-cadherin expression and induce EMT in the cell. However, how Snail achieves this task remains unclear. Understanding this molecular mechanism will help to develop novel agents to disrupt this EMT event for treating metastatic breast cancer.

The study, recently published online in the Journal of Clinical Investigation, identified that Snail interacted with a chromatin modifying enzyme G9a and recruited G9a to the E-cadherin promoter. This action closes the gene structure of E-cadherin and thus results in the suppression of “molecular glue” E-cadherin expression. The findings establish that the interaction of Snail with G9a is an important determinant of metastasis in triple-negative breast cancer.

"This finding has significant clinical ramification, because chemical compounds or agents that can disrupt the interaction of Snail with G9a will have a great therapeutic potential of treating triple-negative breast cancer," said UK's Peter Zhou, principal investigator for the study. "Investigators at the Markey Cancer Center are currently exploring this idea and are keen to develop drugs that can treat triple-negative breast cancer."

http://www.newswise.com/articles/new-study-shows-promise-for-developing-new-treatments-for-breast-cancer#.T2Gmr_i6ekw.facebook

http://www.medicalnewstoday.com/releases/242796.php




Edited by 123Donna - Oct 08 2019 at 11:23pm
DX IDC TNBC 6/09 age 49, Stage 1,Grade 3, 1.5cm,0/5Nodes,KI-67 48%,BRCA-,6/09bi-mx, recon, T/C X4(9/09)
11/10 Recur IM node, Gem,Carb,Iniparib 12/10,MRI NED 2/11,IMRT Radsx40,CT NED11/13,MRI NED3/15

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BCRF-Supported Study Identifies Novel Target in Metastasis

In a new study, BCRF researcher Dr. Andrew Ewald and his team made a discovery that could lead to lifesaving targeted treatments.

Metastasis – the process where cancer spreads to other tissues – is a complex, multi-step process. Most cancer cells do not survive the journey. Those that do, and form new tumors at a different site, are the leading cause of breast cancer deaths.

In an article published in the journal Nature, BCRF investigator and a Play for P.I.N.K. Award recepient Dr. Andrew Ewald made a stunning discovery that may aid in our understanding of metastasis. The BCRF-supported study explained how cancer cells survive with the help of a protein called E-cadherin. Dr. Ewald describes how E-cadherin, which is known to suppress cancer cell invasion – the first step in metastasis – actually promotes the survival of cancer cells that do invade.

“We had a hunch that E-cadherin was playing a role in promoting metastasis, in spite of the fact that it suppresses cancer cell invasion,” Dr. Ewald explained. “This exploratory work could not have been done without BCRF support. It’s an example of how BCRF allows investigators to pursue high-risk, high-reward research and to expand into new directions.”

Dr. Ewald’s intuition was based on the observation that E-cadherin is found on the cancer cells in the primary tumor – as well as those in the metastases.

What is E-cadherin?

E-cadherin is the “glue” that helps maintain tissue structure. It is also the glue that holds tumors together. Loss of E-cadherin in cancer cells allows the cells to break away from the tumor and invade tissue around the tumor, an important first step in metastasis. Because of this, loss of E-cadherin was believed to be a requirement of metastasis.

Dr. Ewald employed sophisticated laboratory technologies to control the expression of E-cadherin in breast cancer cells and tumors. As expected, when E-cadherin was suppressed, tumor cells spread from all borders of the tumor. His experiments went on to show, however, that those tumor cells were less likely to survive afterwards.

Conversely, while the presence of E-cadherin suppressed the cell spreading, it did not completely eliminate it. Furthermore, those cells that did spread, survived and formed new tumors. His experiments further showed that E-cadherin blocked signals that caused tumor cells to die, thereby promoting cancer cell survival and metastasis.

Why is this finding important?

The most common form of invasive breast cancer – invasive ductal carcinoma – retains E-cadherin even when it has metastasized. Understanding how E-cadherin works to promote metastasis could lead to targeted treatment and prevention strategies with the potential to dramatically reduce deaths from metastasis.

What’s next?

Dr. Ewald is not stopping here. He’s now exploring the role of E-cadherin in other aspects of metastasis such as tumor cell dormancy – a state where tumor cells lie sleeping undetectable by current screening methods.  These tumor cells can wake up, sometimes many years after treatment has ended, and form a new tumor.

“Our future research aims to understand how to target the survival signals related to E-cadherin and prevent metastases from forming, thereby saving patients’ lives,” he says.

https://www.bcrf.org/blog/bcrf-supported-study-identifies-novel-target-metastasis

DX IDC TNBC 6/09 age 49, Stage 1,Grade 3, 1.5cm,0/5Nodes,KI-67 48%,BRCA-,6/09bi-mx, recon, T/C X4(9/09)
11/10 Recur IM node, Gem,Carb,Iniparib 12/10,MRI NED 2/11,IMRT Radsx40,CT NED11/13,MRI NED3/15

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