Intertwining of Activin A and XXXX Signaling: Dual Roles in Cancer Progression and Cancer Cell Invasion.

@entity1 @entity0 @entity5 @entity2533 @entity213
In recent years, a significant amount of research has examined the controversial role of activin A in @entity5 . Activin A, a member of the @entity2533 ( @entity2533 ) superfamily, is best characterized for its function during embryogenesis in mesoderm cell fate differentiation and reproduction. During embryogenesis, @entity2533 superfamily ligands, @entity2533 , bone morphogenic proteins (BMPs) and activins, act as potent morphogens. Similar to TGFbs and BMPs, activin A is a protein that is highly systemically expressed during early embryogenesis; however, post-natal expression is overall reduced and remains under strict spatiotemporal regulation. Of importance, normal post-natal expression of activin A has been implicated in the migration and invasive properties of various immune cell types, as well as endometrial cells. Aberrant activin A signaling during development results in significant morphological defects and premature mortality. Interestingly, activin A has been found to have both oncogenic and @entity5 suppressor roles in @entity5 . Investigations into the role of activin A in prostate and @entity0 has demonstrated @entity5 suppressive effects, while in lung and head and @entity213 , it has been consistently shown that activin A expression is correlated with increased proliferation, invasion and poor @entity1 prognosis. Activin A signaling is highly context-dependent, which is demonstrated in studies of epithelial cell @entity5 and the microenvironment. This review discusses normal activin A signaling in comparison to @entity2533 and highlights how its dysregulation contributes to @entity5 progression and cell invasion.
