Decreased stathmin expression does not affect the actions of human choriogonadotropin or epidermal growth factor in Leydig tumor cells.

Abstract

Although hCG and mouse epidermal growth factor (mEGF) activate different signaling systems in a clonal strain of murine Leydig tumor cells (designated MA-10), both compounds ultimately elicit several common effects such as increased steroidogenesis, decreased transcription of the LH receptor gene and attenuation of adenylyl cyclase. A 21-kilodalton protein whose phosphorylation state increases after hCG and mEGF stimulation has previously been described and identified as stathmin. To determine whether stathmin is involved in the signaling pathways of hCG and mEGF, an expression vector containing the full-length stathmin complementary DNA in an antisense orientation was constructed and used to establish two novel clonal MA-10 cell lines that have a decreased level of stathmin expression. Characterization of these mutant cell lines revealed no differences from MA-10 cells or neomycin-resistant subclones of MA-10 cells with respect to the ability of hCG or mEGF to increase steroidogenesis, decrease transcription of the LH receptor, or attenuate the adenylyl cyclase activity. Thus, it appears that stathmin is not involved in mediating the common actions of hCG and mEGF in MA-10 cells.