Syndecan expression regulates cell morphology and growth of mouse mammary epithelial tumor cells.

AUTOR(ES)

Leppä, S

RESUMO

S115 mouse mammary epithelial cells lose their epithelial morphology and become tumorigenic when exposed to steroids. We have recently reported that testosterone exposure results in the suppression of syndecan expression, suggesting that this cell surface proteoglycan may influence S115 cell phenotype. We now report that a similar suppression and morphological response of S115 cells can be achieved by glucocorticoid exposure. We introduced into S115 cells an exogenous gene construct containing the full-length human syndecan cDNA under the control of a glucocorticoid-inducible retroviral promoter, in order to study the effect of syndecan expression on S115 cell behavior. Glucocorticoid-induced re-expression of syndecan in S115 cells restored an epithelial phenotype, while control transfectants and parental S115 cells exhibited an altered, nonepithelial phenotype. Moreover, the S115 cells expressing exogenous syndecan revealed a reduced ability to form colonies in soft agar. Therefore, the maintenance of epithelial morphology and normal growth of S115 cells are dependent on syndecan expression.

Documentos Relacionados

• Translational suppression of syndecan-1 expression in Ha-ras transformed mouse mammary epithelial cells.
• Steroid-induced epithelial-fibroblastic conversion associated with syndecan suppression in S115 mouse mammary tumor cells.
• Serum-free growth of normal and tumor mouse mammary epithelial cells in primary culture.
• Mouse mammary tumor gene int-3: a member of the notch gene family transforms mammary epithelial cells.
• Amplification of mouse mammary tumor virus genomes in non-mammary tumor cells.