The mechanism and significance of E-cadherin, anti-apoptosis B-cell lymphoma-2 protein and sE-cadherin roles in cancer

L. Liu, H. X. Li, X. Q. Lv

Article ID: 5951
Vol 28, Issue 4, 2014
DOI: https://doi.org/10.54517/jbrha5951
Received: 8 January 2015; Accepted: 8 January 2015; Available online: 8 January 2015; Issue release: 8 January 2015

Abstract

Women are most likely to suffer from breast cancer of all the malignant tumors. Its incidence is growing rapidly, which severely threatens the health of females. E-cadherin (E-cad), as the mediator of tumor tissue cells, when adhesion between the cells decreases, can improve the wettability and migration ability of cells, and help cell growth and proliferation in the new area. E-cad serves not only as a cancer inhibitor but also as a cancer promoter. sE-cadherin (sE-cad) is formed as a result of the degradation and exfoliation of N-end extracellular domain of E-cad and its level is closely related to the invasion and metastasis of tumor cells. B-cell lymphoma-2 protein (Bcl-2 protein) is the key regulatory factor for the mitochondria apoptosis pathway during the apoptosis of cells, and it plays an important role in the signal transduction pathway of cell apoptosis. Its abnormal expression may induce disorder of the mechanism. This paper, through the study of the expression and relationship of E-cad, Bcl-2 protein and sE-cad, attempts to explain their expression changes during the development of breast cancer, providing clues clinically useful for further recognition of occurrence and development, early diagnosis, interference and early treatment of breast cancer.


Keywords

breast cancer;E-cad;anti-apoptosis Bcl-2 protein;sE-cad


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Supporting Agencies



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