Differential Regulation of TauT by Calcitriol and Retinoic Acid via VDR/RXR in LLC-PK1 and MCF-7 Cells - Advances in Experimental Medicine and Biology - page 282

Table 27.1 Cell line properties relative to TauT gene expression
MCF-7 LLC-PK1

Tissue Human breast carcinoma Pig kidney proximal tubule

Estrogen Positive Negative

p53 ↑ TauT ↓ TauT

ER ↑ TauT Not active

Estrogen receptor element (ERE) −949 to −954 Not active

E2 ↑ TauT No effect

VDRE/RXR, 1,25(OH) 2 D3/atRA ↓ TauT ↑ TauT

Fig. 27.4 Depiction of the regulation of TauT by VDR/RXR in renal cells

MCF-7 cells were derived from a malignant breast cancer metastatic lesion and as
such tend to grow in a relatively uncontrolled fashion (Diesing et al. 2006 ) . One
response to 1,25(OH) 2 D 3 in MCF-7 cells is to downregulate ER abundance and to
suppress estrogen (E2) action in these cells (Swami et al. 2000 ) . Because a majority
of breast tumors show estrogen-dependent growth, they can be susceptible to anties-
trogen therapy. Vitamins A and D have antiestrogenic action in this cell line, probably
by interaction with the estrogen response element, but they appear to act by differ-
ent mechanisms (Demirpence et al. 1994 ) . Vitamin D and its metabolite, 1,25(OH) 2 D 3 ,
possess both antiproliferative and proapoptotic properties in MCF-7 cells. Estrogen
upregulates VDR and induces ERK 1/2 activation in these cells (Gilad et al. 2005 ) .
Recent information indicates that the antiproliferative action of vitamin D in MCF-7