Biological and biochemical characterization of estrogen-dependent mouse Leydig cell tumors
Journal of Steroid Biochemistry, ISSN: 0022-4731, Vol: 27, Issue: 1, Page: 421-429
1987
- 3Citations
- 2Captures
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Article Description
Leydig cell tumors formed in BALB/c mice were found to be able to be transplanted subcutaneously in the same strain. One of the sublines, called T 22137, showed growth inhibition in response to estrogenization of host mice. The other subline (T 124958-O), which was originally classified as an estrogen-independent line, was observed to contain the low-affinity estradiol binding component in the cytosol fraction. At a later stage of transplantation, however, the growth of this subline was modestly but significantly enhanced by estrogenic stimuli. This alteration was accompanied by appearance of an estrogen receptor-like molecule which was associated with chromatin even in the absence of estrogen stimuli. In the presence of estrogen selection pressure, a new tumor line, designated as T 124958-R, was established, which showed marked estrogen-dependent growth. T 124958-R was found to contain the cytosolic estrogen receptor. The additional difference was that the annulate lamellae were identified only in T 124958-R, but not in T 124958, by electron microscopic studies. The estrogen dependency of T 124958-R was further substantiated by demonstration of an estrogen secretory protein as well as the estrogen-enhanced formation of 5α-steroids. T 22137 showed growth inhibition in tamoxifen-treated mice. The growth of T 124958-R was enhanced by the administration of tamoxifen to mice. This tamoxifen-induced tumor growth was further stimulated by the simultaneous administration of estrogen. These observations would suggest that mouse Leydig cell tumor systems provide us with a valuable model to investigate the influence of estrogen as well as antiestrogen on malignant cells.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0022473187903360; http://dx.doi.org/10.1016/0022-4731(87)90336-0; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0023464017&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/3695489; https://linkinghub.elsevier.com/retrieve/pii/0022473187903360; http://dx.doi.org/10.1016/0022-4731%2887%2990336-0; https://dx.doi.org/10.1016/0022-4731%2887%2990336-0
Elsevier BV
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