Cell lines:
- CTR have been detected in various breast cancer cell (BCC) lines, including MCF-7 and T-47D BCC.
- Calcitonin interaction with CTR led to growth inhibition and prevented c-jun protooncogene induction by EGF and insulin, and
TIMP-1 and
TIMP-2 induction by the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) in T-47D BCC (Lacroix M. et al., 1997).
Tumors:
- 18 primary breast cancers were studied by reverse transcription-PCR for expression of CTR and of the bone proteins
osteopontin (OPN) and
bone sialoprotein (BSP).
OPN and CTR were expressed by each of the tumours, and 7 (39%) additionally expressed an alternate form of CTR, whilst
BSP was expressed by 13 tumours (72%). In situ hybridisation confirmed that expression of
OPN and CTR was confined to the tumour cells (Gillespie M.T. et al., 1997).
Gillespie M.T. et al. (1997) Calcitonin receptors,
bone sialoprotein and
osteopontin are expressed in primary breast cancers. Int. J. Cancer 73, 812-815.
Lacroix M. and Body J.J. (1997) Regulation of c-fos and c-jun expression by calcitonin in human breast cancer cells. Calcif. Tissue Int. 60, 513-519.
Perez-Jurado L.A. et al. (1995) The human calcitonin receptor gene (CALCR) at 7q21.3 is outside the deletion associated with the Williams syndrome. Cytogenet. Cell Genet. 70, 246-249.
