Expressions of Cell Cycle Regulators in Human Colorectal Cancer Cell Lines
Autor: | Marcelo Eidi Nita, Hirokazu Nagawa, Tetsuichiro Muto, Shin Fujii, Takashi Tsuruo, Osamu Tominaga |
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Jazyk: | angličtina |
Rok vydání: | 1997 |
Předmět: |
Cancer Research
Cyclin‐dependent kinase Tumor suppressor gene Esophageal Neoplasms Cyclin‐dependent kinase inhibitor Gene mutation Mouse model of colorectal and intestinal cancer medicine.disease_cause Retinoblastoma Protein Article Cyclin-dependent kinase Cyclins medicine Tumor Cells Cultured Humans Enzyme Inhibitors Cyclin biology Cell Cycle Cell cycle Genes p53 Colorectal cancer Cyclin-Dependent Kinases Oncology Cancer cell Colonic Neoplasms biology.protein Cancer research Tumor Suppressor Protein p53 Carcinogenesis Colorectal Neoplasms |
Zdroj: | Japanese Journal of Cancer Research : Gann |
ISSN: | 1876-4673 0910-5050 |
Popis: | To study the altered mechanisms of cell cycle regulation in colorectal cancer, the expressions of cyclins, cyclin-dependent kinases (CDKs), CDK inhibitors, p53 and retinoblastoma (Rb) protein were analyzed by western blotting in a series of human colorectal cancer cell lines. The colorectal cancer cell lines exhibited various expression patterns of cell cycle regulators, which may reflect differences in the biological characteristics of cancer cells and in the genetic backgrounds of carcinogenesis. A correlation was found between p53 gene alteration and p21 expression, suggesting that p53 gene mutation usually suppresses p21 expression, though p21 expression could be induced via both a p53-dependent and a p53-independent pathway in colorectal cancer. None of the cell lines studied expressed p16 protein, suggesting that inactivation of p16 may be a common alteration in colorectal cancer. Moreover, all the D-type cyclins, especially D2 and D3, were expressed at a high level in most of the cell lines. Loss of p16 expression and increased expression of D-type cyclins promote CDK-mediated Rb phosphorylation. All of the colorectal cancer cell lines studied herein expressed Rb protein, but the growth-suppressive properties of Rb may be inactivated by the loss of p16 expression and increased expressions of D-type cyclins. In view of the pivotal role of Rb in cell cycle regulation, loss of p16 expression and overexpression of D-type cyclins may be critical alterations in colorectal cancer. |
Databáze: | OpenAIRE |
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