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EphA2 Induces Metastatic Growth Regulating Amoeboid Motility and Clonogenic Potential in Prostate Carcinoma Cells

Perhaps the greatest challenge facing modern medicine is to understand and develop effective treatments for cancer. As a disease that has touched the lives of millions, immeasurable amounts of time and money has been dedicated to its eradication. However, cancer is an incredibly complex disease; with hundreds of different variations reacting in different ways depending on the person, finding just one cure seems like a remote possibility. Instead, researchers must work to determine the specific mechanisms of different cancers and then hope they can extrapolate their results to other conditions. EphA2 is a kinase that regulates cell shape, adhesion, and motility that is frequently found over-abundantly in several cancers, such as melanoma, prostate, breast, and colon cancers, as well as lung carcinoma. Several studies have suggested EphA2 plays a role in tumor onset and metastasis, but there is still debate as to the exact part this kinase plays in cancer development. One additional role that has been identified is related to cell migration and invasiveness. EphA2 has been reported to create a scenario where cells can move by a proteolysis-independent strategy, or ameoboid motility, and this was the focus of the study conducted by Taddei et al.

By stably silencing EphA2 expression in an aggressive metastatic prostate carcinoma, Taddei and this research team were able to take a closer look at the role of EphA2 in cancer development.  One of the ways they did this was to look at the matrix metalloproteinases (MMPs), a family of zinc-dependent endopeptidases known to play a key role in the invasion and metastasis of different cancers. They did this using the Amplite Universal Fluorimetric MMP Activity Assay Kit. This allows researchers to study the general activity of an MMP enzyme, which can help determine the state of invasion or metastasis.

After conducting this study, Taddei et al. found that EphA2 does in fact greatly affect prostate carcinoma cell motility style by encouraging an amoeboid movement. They also found it to be ineffective on transendothelial migration, adhesion onto extracellular matrix proteins, and on resistance to anoikis, something able to be determined thanks to the robust results and readings derived from the Amplite Universal Fluorimetric MMP Activity Assay Kit. Since it is virtually impossible to track the activity of a single MMP substrate, being able to accurately measure the activity of a group of substrates proves invaluable to this type of research. The team also found that EphA2 regulates the clonogenic potential of prostate carcinoma, thereby increasing anchorage-independent growth and self-renewal, prostasphere formation, tumor onset, dissemination to bone, and growth of metastatic colonies. In conclusion, the results of this study are quite groundbreaking, as they provide a much more thorough understanding of the way EphA2 affects the onset and development of prostate cancer. This is the type of research that can redirect treatment efforts, as it provides significant empirical evidence that targeting EphA2 could help mitigate the growth of aggressive prostate cancers, and perhaps others, taking one more step towards finding effective treatments for cancer.

Related Link:

Taddei, Maria Letizia, et al. "EphA2 induces metastatic growth regulating amoeboid motility and clonogenic potential in prostate carcinoma cells.Molecular Cancer Research 9.2 (2011): 149-160.

Original created on August 17, 2017, last updated on August 17, 2017
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