The Role of E-Cadherin in Breast Cancer

Introduction

E-cadherin plays a significant role in regulating the growth of breast cancer in the human body. E-cadherin is a glycoprotein, which comprises of three main structural elements including a single transmembrane connected with a cytoplasmic element and an extracellular component.  The extracellular component of E-cadherin is important for cell-cell adhesion and correct folding. The main function of E-cadherin concerns the epithelial cells where it performs cell-cell adhesion as well as suppresses invasion (Hollestelle, et al., 2013). The conformation of E-cadherin is enabled after the binding of Ca2+ where it becomes negatively charged. The maintenance of the Cadherin-catenin component and its connection to the actin filaments is significant to inhibit individual epithelial cells movement and enhance homeostatic tissue frameworks. E-cadherin is the main component of Adherens Junction (AJ) that is essential in promoting cell-cell contact of the epithelium cells in the human body (Chao, Wu, Shepard, & Wells, 2012). Thus, the decrease of E-cadherin would obviously lead to the dissemination of cancer cells as well as the growth of the tumor. It implies that E-cadherin plays a major role in influencing the growth and development of cancer among the humans (Ribeiro, et al., 2013). Therefore, this paper provides important information for understanding the role of E-cadherin in influencing the rate of breast cancer.

Discussion of Findings

Several researches have been conducted to study the impact of E-cadherin on the growth of breast cancer among the patients. The cell-cell adhesion function of E-cadherin helps in inhibiting the development of cancer cells. Apart from cell-to-cell adhesion, E-cadherin is involved in various signaling ways to control the growth of breast cancer cells (Van Horssen, et al., 2012). Its loss contributes to the activation of signals, which initiate the epithelial mesenchymal transition (EMT). Some of the signaling ways include EGFR, Wnt signaling, and Rho GTPases. Within the Wnt signaling, free catenins would accumulate within the cytoplasm to promote the non-functional adenomatous polyposis col (APC). High quantity of catenins moves into the nucleus leading to the expression of Wnt target genes (Horne, et al., 2014). The activation of these genes contributes to the increase in cell proliferation and the progression of breast tumor. Thus, it is expected that E-cadherin could suppress Wnt by sequestering the catenin in the cell to contact locations. It helps reduce the growth of the cancer cells within the breasts, more so among women.

Using the modulation of mitogenic signaling, E-cadherin can influence tumorigenesis, which enhances the development of cancer. The perspective is supported by the fact that cadherin adhesion leads to cell proliferation within the lung carcinoma cells (Cheung, Gabrielson, Werb, & Ewald, 2013). It implies that E-cadherin adhesion could inhibit the growth of the cancer cells. A number of studies have proved that E-cadherin has the potential to control the growth of cancer cells through the EGF receptor. Matteucci, et al. (2013) found out that E-cadherin integrates with the EGF receptor at the cell contacts and can interact with the EGF receptor. This assists in regulating the modulate signaling of the cancer cells.

Also, E-cadherin could reduce the cell responsiveness to the stimulation by the EGF cells. As measured by cell proliferation, the inhibition of cell responsiveness leads to the decrease in the number of the cancer cells (Canel, Serrels, Frame, & Brunton, 2013). It is also important to understand that the reduced expression of E-cadherin is regarded as the main factor that causes the overall dysfunction of cell-cell process leading to cancer invasion and metastasis (Kelpsch, et al., 2012). Breast cancer comprises of the epithelial cells, which determine the level of cancer metastasis. The progression of a tumor has different stages that can be influenced by E-cadherin expression (Pinto, Widodo, Waltham, & Thompson, 2013). The research on E-cadherin has overlooked the insights on oncogenesis process and its impacts on breast cancer growth. 

Moreover, E-cadherin works as a tumor suppressor, and the regulation of E-cadherin can be recorded in various cancer situations. The process of genetic mutation is one of the main processes of silencing tumor suppressor genes. However, the studies of familiar cancer indicated that alterations within the germlines lead to inherent cancer conditions. Van Roy (2014) provided adequate evidence that the inactivation and absence of E-cadherin lowers cell-cell adhesion thus inducing cell proliferation and inflammation among others. These changes are responsible for the breast cancer development and growth (Tang, Xu, Zhang, & Zhao, 2012). E-cadherin also contributes to the cell connection and the modulation of epithelial cells in the breasts. Such connections are critical in minimizing the expression and activation of breast cancer cells. It is assumed that alterations in E-cadherin indicate the pathological situation of breasts.

Conclusion

In summary, E-cadherin is useful in inhibiting the growth of the breast cancer cells. The adhesion cell element of E-cadherin is reflected on the lateral surfaces of the normal epithelial and could hide in the breast cancers tumors. The absence of E-cadherin could be postulated to enhance cancer cells detachment from the tumor, which leads to metastases. The expression of other cells’ inner surfaces could interfere with the adhesion role of E-cadherin. The cell adhesion of E-cadherin could be favored by improving the rich complexity of its structures, which enhances the regulation of tumor cells proliferation. E-cadherin ensures the stability of the epithelial tissues and homeostasis. It helps in the formation of adherence junctions. Gene therapy is instrumental in preventing the downregulation of E-cadherin. Some of the processes include mutations and repression of genes useful in stimulating the adhesion of E-cadherin and its complex formations. The contribution of E-cadherin to Wnt signaling is useful in regulating cellular responses normally creating external signals. Therefore, E-cadherin is important in reducing the progression of the breast tumor and thus hindering the growth of breast cancer.

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