Title : Induction of retinoid resistance in breast cancer cells by overexpression of cJun.

Pub. Date : 1997 Oct 15

PMID : 9377582






3 Functional Relationships(s)
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1 The c-jun-transfected MCF7 cells had increased basal AP-1 transactivation activity and increased expression of AP-1-regulated genes but were resistant to the antiproliferative effects of atRA. Tretinoin Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
2 However, MCF7 cells transfected with a deletion mutant of c-jun, TAM-67, which lacks most of the amino-terminal transactivation domain of cJun and is unable to activate AP-1-dependent gene expression, were sensitive to the growth-inhibitory effects of atRA. Tretinoin Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens
3 However, retinoic acid responsive element DNA binding activity was intact in c-jun-transfected cells. Tretinoin Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens