objective(s):n-myc downstream regulated gene 2 (ndrg2) is a candidate gene for tumor suppression. the expression of ndrg2 is down-regulated in several tumors including lung cancer. the aim of this study was to explore the effect of ndrg2 overexpression on invasion, migration, and enzymatic activity of matrix metalloproteinase-2 (mmp-2) and -9 (mmp-9) in human lung adenocarcinoma a549 cells.  ma...

background: radiation therapy is among the most conventional cancer therapeutic modalities with effective local tumor control. however, due to the development of radio-resistance, tumor recurrence and metastasis often occur following radiation therapy. in recent years, combination of radiotherapy and gene therapy has been suggested to overcome this problem. the aim of the current study was to e...

OBJECTIVES The aim of this study was to examine the expression of the N-myc downstream-regulated gene 1 protein in benign and malignant lesions of the thyroid gland by immunohistochemistry. INTRODUCTION N-myc downstream-regulated gene 1 encodes a protein whose expression is induced by various stimuli, including cell differentiation, exposure to heavy metals, hypoxia, and DNA damage. Increased...

The proto-oncogene c-myc (myc) encodes a transcription factor (Myc) that promotes growth, proliferation and apoptosis. Myc has been suggested to induce these effects by induction/repression of downstream genes. Here we report the identification of potential Myc target genes in a human B cell line that grows and proliferates depending on conditional myc expression. Oligonucleotide microarrays we...

Adenovirus E1A drives oncogenesis by targeting key regulatory pathways that are critical for cellular growth control. The interaction of E1A with p400 is essential for many E1A activities, but the downstream target of this interaction is unknown. Here, we present evidence that the oncoprotein transcription factor Myc is the target of this interaction. We show that E1A stabilizes Myc protein via...

Mutations in components of the Wnt signaling pathway initiate colorectal carcinogenesis by deregulating the beta-catenin transcriptional coactivator. beta-Catenin activation of one target in particular, the c-Myc proto-oncogene, is required for colon cancer pathogenesis. beta-Catenin is known to regulate c-Myc expression via sequences upstream of the transcription start site. Here, we report th...

This study addresses whether pathological levels of cyclic strain activate the c-Myc promoter, leading to c-Myc transcription and downstream gene induction in human umbilical vein endothelial cells (HUVEC) or human aortic endothelial cells (HAEC). mRNA and protein expression of c-Myc under physiological (6-10%) and pathological cyclic strain conditions (20%) were studied. Both c-Myc mRNA and pr...