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2 "Cell cycle control genes"
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Expression of Cell Cycle Control Genes in Korean Gastric Cancer Cell Lines
C C Lim, I H Kim, J W Cho, W K Baek, S I Suh, M H Suh, J W Park, J S Kang, S S Sohn
J Korean Cancer Assoc. 2000;32(2):279-287.
AbstractAbstract PDF
PURPOSE
In order to elucidate the roles of the cell cycle control genes in the carcinogenesis of Korean gastric cancer, the expressions of cyclin A, Dl, E, p16INK4a and Rb in Korean gastric cancer cells were investigated in this study.
MATERIALS AND METHODS
The expression patterns of major cell cycle control genes in Korean gastric cancer cells (SNU1, 5, 216, 484, 601, 620, 638, 668, 710) were analysed by using western blot and reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS
In most of the gastric cancer cells investigated, the overexpressions of cyclin A and hyperphosphorylated Rb, and markedly decreased expression of p16INK4a were observed. Over-expression of cyclin E was also observed in SNU1, 484, 601 and 638 gastric cancer cells.
CONCLUSION
Considering all these findings, the following model of the gastric catcinogenesis caused by the altered expressions of the cell cycle control genes can be postulated: over-expressions of cyclin A and E cause acceleration of Rb phosphorylation, inactivation of Rb functions and acceleration of Gl/S transition of the cells; decreased expression of pl6INK4a causes inadequate inhibition of cyclin-CDK and further acceleration of Rb phosphorylation; consequently, Rb inactivation, Gl shortening, inappropriate cell division and decreased function of the maintenance of genomic stability occurs. All these abnormalities should contribute to the carcinogenesis of Korean gastric cancer cells.
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Expressions of Cell Cycle Control Genes in Human Uterine Cervical Cancer Cells
Jung Geol Ahn, Tae Seong Lee, Jae We Cho, Won Ki Baek, Seong Il Suh, Min Ho Suh, Jong Wook Park, Soon Do Cha
J Korean Cancer Assoc. 2000;32(1):110-119.
AbstractAbstract PDF
PURPOSE
Recently, many aspects of biological functions of cyclins, cyclin-dependent kinases (CDKs), CDK inhibitors and Rb gene have been reported, and the cell cycle control genes are considered to act important roles in tumorigenesis. In this study, the expression patterns of major cell cycle control genes (cyclin A, B, C, Dl, E, E2F, p16INK4a, p21WAF1 and Rb) in various human cervical cancer cells were analysed to elucidate the impacts of the cell cycle control genes on the carcinogenesis of human cervical cancer.
MATERIALS AND METHODS
The expression patterns of major cell cycle control genes in HT-3, C33-A, HeLa, C4-II, SiHa and CaSki human uterine cervical cancer cells were analysed by using western blot and reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS
In most of the cervical cancer cells tested, the overexpressions of cyclin A, E, E2F and markedly decreased expression of Rb tumor suppressor proteins were observed. By comparing RNA and protein expressions in each cancer cells, the mechanisms of increased expressions of cyclin A, E and decreased expression of Rb were elucidated as post-translational controls.
CONCLUSION
The cervical carcinogenesis caused by the altered expressions of the major cell cycle control genes can be hypothesized as follows: overexpressions of cyclin E and A cause acceleration of Rb phosphorylations and E2F overexpression; increased E2F function accelerates G1/S transition of the cells; compensatory increase of p16 expression cannot stop the cells in Gl phase because Rb expression is severely decreased; consequently, loss of Rb function, 61 shortening, inappropriate cell division and decreased function of the maintenance of genomic stability occur. In addition to these alterations, loss of p53 functions further accelerate instability of genome and decrease the sus- ceptability to cell death. Furthermore, overexpression of Bc12 protects these abnormal cells from apoptosis. All these derangements of cell cycle control should contribute to the human cervical carcinogenesis.
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