Steroid hormones estrogen and progesterone regulate many biological events including behaviour, reproduction, development, cell differentiation and apoptosis. These hormones and their derivatives are used in contraceptive pills and in the treatment of infertility and menopausal symptoms. They also play a role in many illnesses such as breast and endometrial cancer and osteoporosis. These hormones require specific intracellular proteins termed receptors, to which they bind. In addition, a set of regulatory proteins termed coregulators, which are further divided into coactivators, corepressors and cointegrators, are needed before the transcription of target genes is either activated or silenced. However, the detailed mechanisms of how steroid hormone response is achieved and regulated, are not yet known. Breast cancer is the most common cancer among Finnish women; approximately 3,800 new breast cancers were diagnosed in Finland in 2003. Antiestrogens tamoxifen and toremifene are synthetic drugs, which are used in the treatment of this disease. Estrogen and progesterone receptor levels are measured in breast cancer samples in order to identify patients who will benefit from these drugs. Unfortunately, many patients fail to benefit from antiestrogen treatment after initial response despite of receptor-positivity and the drug may ultimately even stimulate the tumour growth, which is an important problem clinically. This study was undertaken in order to study the expression and hormonal regulation of steroid hormone receptors and coregulators both in normal murine and in human breast cancer cells. In addition, cell culture models of endocrine-resistant and hormone-independent breast cancer were established and the questions as to how and why breast cancer cells become drug-resistant were studied. According to the results, both progesterone receptor (PR) and its coactivator, GRIP1, are both widely expressed in murine tissues and the expression pattern is cell-specific. Urogenital, gastrointestinal, endocrinological, immunological and cardiovascular organs, respiratory tract and skin contain PR and progestrone may also regulate the blood flow in some organs. Almost all PR-expressing cells also express GRIP1. Striated muscle and thyroid gland cells did not express either PR or GRIP1. PR was expressed only in the nuclei of cells, and although GRIP1 was expressed predominantly in the nuclei, cytoplasmic expression was also seen. PR expression was estrogen-dependent and -regulated in some tissues, while GRIP1 expression nor its subcellular localization were not dependent on estrogen. Decrease in the expression of PR and G protein-coupled receptor 30 (GPR30), which is a member of a large family of cell surface receptors, and increase in the expression of coactivator AIB1 were seen in antiestrogen-resistant breast cancer cells. Toremifene did not regulate any of the steroid hormone receptors or coregulators studied, but in addition to being a competitive inhibitor of estradiol in binding to estrogen receptors, toremifene may also act through membrane receptor GPR30. GPR30 may also be a potential new marker for predicting response to antiestrogen therapy. Furthermore, the development of hormone-independency in breast cancer cells is associated with changes in the levels of steroid hormone receptors and coregulators. In summary, new information about cell-specific expression of steroid hormone receptors and coregulators and about their hormonal regulation in normal and breast cancer cells was obtained in this study. Furthermore, some new data about development of antiestrogen resistance and a potential new mechanism of the action of toremifene were found.