MAP17 overexpression is a common characteristic of carcinomas

• Published in: Carcinogenesis (New York) 2007-08, Vol.28 (8), p.1646-1652
• Main Authors: Guijarro, Maria V., Leal, Juan F.M., Fominaya, Jesus, Blanco-Aparicio, Carmen, Alonso, Soledad, Lleonart, Matilde, Castellvi, Josep, Ruiz, Lidia, Ramon y Cajal, Santiago, Carnero, Amancio
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cancer; Carcinogenesis, carcinogens and anticarcinogens; Carcinoma - metabolism; Carcinoma - pathology; Cell Line, Tumor; Colonic Neoplasms - metabolism; Humans; Lung Neoplasms - metabolism; Male; Medical sciences; Membrane Proteins - biosynthesis; Membrane Proteins - genetics; Oncogenes - physiology; Organ Specificity - genetics; Promoter Regions, Genetic; Prostatic Neoplasms - metabolism; Tumor Cells, Cultured; Tumors; Xenopus
• ISSN: 0143-3334; 1460-2180
• DOI: 10.1093/carcin/bgm083

We undertook a large-scale genetic screen to identify genes able to alter the cellular response to physiological signals and provide selective advantage once tumorigenesis has begun. We identified MAP17, a small 17 kDa non-glycosylated membrane protein previously identified, being overexpressed in carcinomas. We found that MAP17 is overexpressed in a great variety of human carcinomas. Immunohistochemical analysis of MAP17 during cancer progression shows, at least in prostate and ovarian carcinomas, that overexpression of the protein strongly correlates with tumoral progression (P < 0.0001). Many tumor cells also express MAP17 and its expression does not correlate with expression of SCL, a neighbor gene reported to be co-expressed in some hematopoietic cell lines. SCL neither is expressed in most MAP17-positive tumors, indicating the independent transcription of MAP17, at least in carcinomas. We cloned 5′ genomic region to MAP17 and described the minimal promoter necessary to produce independent activation of MAP17. Moreover, we have found that MAP17 promoter is activated by oncogenes. Taken together, our data show an independent activation of MAP17 promoter that can be driven by oncogenes and that might explain the common overexpression of MAP17 in human carcinomas.