AI Article Synopsis
- - Neuroblastoma is the most common type of extracranial tumor found in children, and high levels of activin A are linked to better outcomes, although the exact mechanisms are not fully understood.
- - Research shows that increased keratoepithelin expression in neuroblastoma cells reduces their ability to stick together and to extracellular matrix proteins, while also slowing down cell growth and movement both in lab conditions and in living organisms.
- - Additionally, a microarray analysis revealed specific genes regulated by keratoepithelin that may influence these changes, suggesting that keratoepithelin could play a positive role in how neuroblastoma develops and progresses.
Article Abstract
Neuroblastoma is the most common extracranial childhood tumor. High expression of activin A is associated with a favorable prognosis, but the contributing mechanisms have remained unclear. Our previous demonstration of the activin A-mediated up-regulation of keratoepithelin led to the consideration that keratoepithelin could modulate neuroblastoma growth and/or progression. We report here that enhanced keratoepithelin expression in human neuroblastoma cells suppresses neuroblastoma cell cohesion and adhesion to various extracellular matrix proteins and that it inhibits neuroblastoma cell proliferation and invasion in vitro and in vivo. Using microarray analysis, we identified several keratoepithelin-regulated genes that may contribute to these biological changes. Together with the observation that keratoepithelin is expressed in human neuroblastomas in vivo, our data suggest that keratoepithelin could play a beneficial role in neuroblastoma development and/or progression.
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| http://dx.doi.org/10.1158/0008-5472.CAN-05-3049 | DOI Listing |
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