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J Biol Chem, Vol. 273, Issue 28, 17573-17578, July 10, 1998
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From the Departments of A partial resistance to the growth inhibitory
influence of 1,25-dihydroxyvitamin D3 is apparent
when immortalized keratinocytes are transformed by the ras
oncogene. The vitamin D receptor (VDR) was isolated, analyzed, and
found to be identical in normal, immortalized, and
ras-transformed keratinocytes. Subsequently, nuclear
extracts from immortalized and ras-transformed
keratinocytes were analyzed in gel mobility shift assays utilizing
labeled vitamin D response elements or thyroid hormone response
elements. A specific protein·DNA complex that was shown to contain
VDR using an anti-VDR antibody was identified in both types of
extracts; however, the addition of an anti-retinoid X receptor (RXR)
antibody identified RXR in the complex of both normal and immortalized
keratinocyte cell extracts, but not in ras-transformed
keratinocytes. Furthermore, transfection of ras-transformed
keratinocytes with wild-type human RXR Medicine and
¶ Physiology, McGill University, Montreal, Quebec H3A 1A1, Canada
and the Laboratory of Molecular Oncology, NCI-Frederick Cancer
Research and Development Center, National Institutes of Health,
Frederick, Maryland 21702
rescued VDR·RXR and thyroid
hormone receptor·RXR complexes as demonstrated by a supershift in the
presence of the anti-RXR antibody. Both cell lines were found to
express RXR message in equal amounts. Western blot analysis revealed
that RXR protein from ras-transformed keratinocytes was
indistinguishable from that from immortalized keratinocytes and from
control cells. These results suggest a causal relationship between
resistance to the growth inhibitory influences of 1,25-dihydroxyvitamin
D3 and disruption of the VDR·RXR complex in malignant
keratinocytes.
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