Egr-1 negatively regulates human tumor cell growth via the DNA-binding domain.

摘要: Abstract Human HT1080 fibrosarcoma cells, subclone H4, express little or no Egr-1 (Zif/268, Krox 24), an early growth response gene encoding a transcription factor. Phorbol ester (but not serum) treatment only can elicit small increase in expression contrast to the normally rapid, high transient of observed after addition wide range stimulating agents normal immortalized cell lines. Because several human tumor lines Egr-1, we tested hypothesis that this loss was causal transformation. We report here exogenous mouse H4 cells inhibits transformed dose-dependent manner and significantly suppresses tumorigenicity athymic mice. By overexpression fragment is responsible for its DNA-binding activity, zinc-finger domain, show domain has similar activity. Moreover, antisense mRNA increases character cells. One possible conclusion endogenous Egr-1-like genes perform growth-regulatory functions. Other are also suppressed by including ZR-75-1 breast carcinoma, U251 glioblastoma, lesser extent, SAOS-2 osteosarcoma These results surprising light “early response” but extend our earlier suppression v-sis-transformed NIH3T3