The RB tumor suppressor positively regulates transcription of the anti-angiogenic protein NOL7.

The expression of the angiogenic phenotype is regulated by a balance of pro-angiogenic and anti-angiogenic factors released into the tumor microenvironment. Nuclear protein 7 (NOL7), a novel tumor suppressor, acts as a master regulator of angiogenesis by downregulating pro-angiogenic factors and upregulating anti-angiogenic factors. Using cervical cancer as a model of investigation, we have previously shown that loss of NOL7 mRNA and protein expression is observed as early as the premalignant phase.

Dual inhibition of vascular endothelial growth factor receptor and epidermal growth factor receptor is an effective chemopreventive strategy in the mouse 4-NQO model of oral carcinogenesis.

Despite recent therapeutic advances, several factors, including field cancerization, have limited improvements in long-term survival for oral squamous cell carcinoma (OSCC). Therefore, comprehensive treatment plans must include improved chemopreventive strategies. Using the 4-nitroquinoline 1-oxide (4-NQO) mouse model, we tested the hypothesis that ZD6474 (Vandetanib, ZACTIMA) is an effective chemopreventive agent.

Identification and characterization of the human NOL7 gene promoter.

NOL7 is a candidate tumor suppressor gene that localizes to 6p23, a chromosomal region frequently associated with loss of heterozygosity in a number of malignancies including cervical cancer (CC). Re-expression of NOL7 in CC cells suppresses in vivo tumor growth by 95% and alters the angiogenic phenotype by modulating the expression of VEGF and TSP1. Here, we describe the determination of two NOL7 transcriptional start sites (TSS), the cloning of its regulatory promoter region, and the identification of transcription factors that regulate its expression.

Alteration of gene expression in human cells treated with the agricultural chemical diazinon: possible interaction in fetal development.

Agricultural chemicals frequently alter human health or development, typically because they have endocrine agonist or antagonist activities and alter hormone-regulation of gene expression. The insecticide, diazinon, was evaluated for gene expression disrupting activity using MCF-7 cells, an estrogen-dependent human cell line, to examine the capacity of the insecticide to disrupt gene expression essential for morphological development, immune system development or function, and/or central nervous system development and function. MCF-7 cells were treated with 30, 50 or 67 ppm diazinon, and gene expression was measured in treated cells compared to expression in untreated or estrogen-treated cells.