Activin receptor signaling regulates prostatic epithelial cell adhesion and viability.

Mutational changes coupled with endocrine, paracrine, and/or autocrine signals regulate cell division during carcinogenesis. The hormone signals remain undefined, although the absolute requirement in vitro for fetal serum indicates the necessity for a fetal serum factor(s) in cell proliferation. Using prostatic cancer cell (PCC) lines as a model of cancer cell proliferation, we have identified the fetal serum component activin A and its signaling through the activin receptor type II (ActRII), as necessary, although not sufficient, for PCC proliferation.

Redox active iron accumulation in aceruloplasminemia.

Aceruloplasminemia is an autosomal recessive disorder characterized by a ceruloplasmin gene mutation and defective or absent ceruloplasmin function. Because ceruloplasmin functions in iron transport and storage, aceruloplasminemia leads to excessive iron accumulation systemically and within the CNS. The type and form of iron deposited is unclear and while oxidative stress was hypothesized as a potential mechanism of cytotoxicity in this disorder, direct evidence linking oxidative stress to the underlying genetic defect has not been provided.