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- Title
Production of VEGF and expression of the VEGF receptors Flt-1 and KDR in primary cultures of epithelial and stromal cells derived from breast tumours.
- Authors
Speirs, V; Atkin, S L
- Abstract
Production of vascular endothelial growth factor (VEGF) and expression of its receptors Flt-1 and KDR was determined in primary cultures of separated epithelial and stromal-enriched cultures derived from ten primary human breast carcinomas. By enzyme-linked immunosorbent assay, epithelial cells produced a mean VEGF of 33 ± 7 pg ml[SUP-1] μg[SUP-1] RNA (range 11-70). Stromal cells produced similar levels, with a mean of 48 ± 11 pg ml[SUP-1] μg[SUP-1] RNA (range 7-92). This was significantly greater than the amount produced by similar cultures derived from normal breast tissue (epithelial mean 19 ± 5 pg ml[SUP-1] μg[SUP-1] RNA, range 9-34, P < 0.05 vs tumour epithelial culture; stromal mean 26 ± 8 pg ml[SUP-1] μg[SUP-1] RNA, range 3-56). Flt-1 and KDR receptors were analysed by semi-quantitative reverse transcription polymerase chain reaction. Flt-1 was expressed by four of six epithelial and five of six stromal cultures. When expressed by both cell types, Flt-1 appeared to be significantly more abundant on stromal cells compared with epithelial cultures. Only a single tumour, a lobular carcinoma, failed to express Flt-1 on either cell type. With KDR, the reverse was true with constitutive expression of this receptor by epithelial cultures and zero or reduced (3/6) expression by stromal cultures. Differences in the expression pattern of VEGF receptors may reflect a differential response to VEGF by specific cell types. Thus, production of VEGF and expression of VEGF receptors Flt-1 and KDR by breast cancer epithelial and stromal cells suggests that VEGF may fulfil not only an angiogenic role, but also play a fundamental role as an autocrine/paracrine regulator in breast cancer, thereby facilitating tumour proliferation and subsequent invasion.
- Subjects
GROWTH factors; VASCULAR endothelium
- Publication
British Journal of Cancer, 1999, Vol 80, Issue 5/6, p898
- ISSN
0007-0920
- Publication type
Article
- DOI
10.1038/sj.bjc.6690438