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Control of growth of estrogen-sensitive cells: role for alpha-fetoprotein.
Author(s) -
Ana M. Soto,
Carlos Sonnenschein
Publication year - 1980
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.77.4.2084
Subject(s) - cell culture , biology , alpha fetoprotein , cell growth , endocrinology , medicine , estrogen , growth inhibition , microbiology and biotechnology , andrology , biochemistry , cancer research , genetics , hepatocellular carcinoma
The role played by alpha-fetoprotein (AFP) during the perinatal period in rats has not yet been ascertained despite earlier suggestions that this plasma protein affected the multiplication, in an "in animal-in culture" system of tumor cells that are stimulated by estrogen (E) for growth. To test this inference developed from our previous work, AFP was purified by reverse affinity chromatography to homogeneity by electrophoretic and immunochemical criteria. Purified AFP was added at different concentrations to horse serum-supplemented medium which by itself is able to allow maximal exponential growth of a rat pituitary tumor cloned cell line C29RAP. These cells carry estrophilins and their growth is stimulated by E in animals but not in culture. At 3 mg/ml in culture media, AFP prevented growth of C29RAP cells; the effect was dose dependent. F4C1, a rat pituitary cloned cell line that carries estrophilins but shows autonomous behavior when injected into male and female Fisher rats, was not affected in cultured by comparable concentrations of AFP in the culture media. The effect of AFP on the growth of E-sensitive cells in culture was not reversed by E administration. We conclude from these experiments that (i) AFP is a specific inhibitor of the cell multiplication of cells that are E-sensitive for growth (as defined in this presentation), (ii) estrophilins seem not to play a significant role in this inhibition, and (iii) E appears not to be a growth-promoting hormone per se.

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