“Non-hypercalcemic” analogs of 1α,25 dihydroxy vitamin D augment the induction of creatine kinase B by estrogen and selective estrogen receptor modulators (SERMS) in osteoblast-like cells and rat skeletal organs

Less calcemic Vitamin D analogs enhance creatine kinase specific activity and modulate responsiveness to gonadal steroids in the vasculature

“…This finding also complements our previous findings in human vascular smooth muscle cells in vitro, in which pretreatment with the Vitamin D JKF increased both ER␣ mRNA and protein expression [8]. These results also resemble observations in cultured human bone cells, in which pretreatment with JKF or CB significantly up regulated the response to E 2 in all female-derived cells and to DHT in mature male-derived cells [22][23]. Vitamin D was also reported to induce ER␣ expression in two prostate cancer cell lines [24].…”

Treatment with non-hypercalcemic analogs of 1,25-dihydroxyvitamin D3 increases responsiveness to 17β-estradiol, dihydrotestosterone or raloxifene in primary human osteoblasts

“…However, in both mature and older males, JKF increased basal CK specific activity. Pretreatment with any of the analogs upregulated the responses to estrogen in our human osteoblast cell system as it had in ROS 17/2.8 cells [18,23] or in prepubertal rat diaphyseal bone [6,7]. The up regulation of androgen action (Fig.…”

“…We reported that multiple treatments with "non-hypercalcemic" analogs of Vitamin D, such as MC 1288, CB 1093, EB 1089 and the demonstrably non-calcemic JKF 1624 F2-2 [22] stimulated the specific activity of CK in ROS 17/2.8 osteoblast-like cells [18,23]. Moreover, pretreatment of skeletal-derived cells with these analogs upregulated both responsiveness and sensitivity to E 2 [23] and SERMS [6].…”

“…We have studied the interaction of Vitamin D analogs and estrogens in a rat model [6,7] using the increase in the specific activity of creatine kinase (CK) as a response marker. The brain type (BB) isoenzyme of creatine kinase, part of the "energy buffer" system, which regulates the cellular concentration of ATP and ADP, is the major component of the "E 2 -induced protein" of rat uterus [8] and other tissues containing estrogen (E 2 ) receptors [9].…”

Vitamin D, tamoxifen and β-estradiol modulate breast cancer cell growth and interleukin-6 and metalloproteinase-2 production in three-dimensional co-cultures of tumor cell spheroids with endothelium

“…It is well known that the antiproliferative activity of vitamin D may be connected with regulation of ER expression. While estrogen stimulates the growth of ER + VDR + human tumor breast cancer, vitamin D inhibits it (Somjen et al, 2000). TAM antagonizes the action of β-estradiol when administered together with the steroid and therefore may also influence VDR receptor status, changing tumor cell sensitivity to the action of vitamin.…”