SEL1L Affects Human Pancreatic Cancer Cell Cycle and Invasiveness through Modulation of PTEN and Genes Related to Cell-Matrix Interactions
| Autor: | Enrico Fontanella, Monica Cattaneo, Ida Biunno, Domenico Delia, Cristina Canton |
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| Rok vydání: | 2005 |
| Předmět: |
Cancer Research
Matrix metalloproteinase inhibitor lcsh:RC254-282 Extracellular matrix Downregulation and upregulation Pancreatic tumor Cell Line Tumor Gene expression medicine Humans PTEN Neoplasm Invasiveness extracellular matrix-related genes TIMP1 Tissue Inhibitor of Metalloproteinase-2 Tissue Inhibitor of Metalloproteinase-1 biology PTEN Phosphohydrolase Proteins Cell cycle lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens SEL1L medicine.disease Cell biology Gene Expression Regulation Neoplastic Pancreatic Neoplasms siRNA biology.protein cell cycle cancer invasion Research Article |
| Zdroj: | Neoplasia: An International Journal for Oncology Research, Vol 7, Iss 11, Pp 1030-1038 (2005) |
| ISSN: | 1476-5586 |
| DOI: | 10.1593/neo.05451 |
| Popis: | Previously, it was reported that SEL1L is able to decrease the aggressive behavior of human pancreatic tumor cells both in vitro and in vivo. To gain insights into the involvement of SEL1L in tumor invasion, we performed gene expression analysis on the pancreatic cancer cell line Suit-2 subjected to two complementary strategies: upregulation and downregulation of SEL1L expression by stable transfection of the entire cDNA under an inducible promoter and by RNA-mediated interference. SuperArray and real-time analysis revealed that SEL1L modulates the expression of the matrix metalloproteinase inhibitors TIMP1 (P < .04–.03) and TIMP2 (P < .03–.05), and the PTEN gene (P < .03―.05). Gene expression modulations correlate with the decrease in invasive ability (P < .05) and in accumulation of SEL1L-expressing cells in G1. Taken together, our data indicate that SEL1L alters the expression of mediators involved in the remodeling of the extracellular matrix by creating a microenvironment that is unfavorable to invasive growth and by affecting cell cycle progression through promotion of G1 accumulation. |
| Databáze: | OpenAIRE |
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