| Summary: | 碩士 === 國防醫學院 === 病理及寄生蟲學研究所 === 87 === Telomerase, a ribonucleoprotein, compensates for the continued shortening telomere length by adding hexameric (TTAGGG) repeat to the telomeric ends of the chromosomes. Telomerase activity is expressed in almost all malignant tumors, but is rarely detected in normal somatic cells. Activity is high in the actively cycling culture and low in the quiescent differentiated cells. Telomerase and telomeres have been shown to be involved in the control of cell proliferation, the regulation of cell senescence and the unlimited proliferation capacity of malignant cells. Deregulation of the cell cycle by abnormal expression of same cell cycle regulatory proteins is a common finding in malignant and might be a prerequisite for cancer development. In Hepatocellularcarcinoma (HCC) cell lines, cell cynchronized at G1; G1/S; G2/M; M and G1/S phase by MTX; Thymidine; Doxorubicin; Nocodazole and 5-FU chemical agents, and detected the telomerase activity by TRAP assay. The results showed that the cell cycle transition was different the other cell lines, and could detect the telomerase activity in all cell cycles but the highest in M phase. We also investigated the expression of cell cycle regulators by ELISA, Western blot, Immunocytochemical stain and correlation with the telomerase activity. The experimental data showed that increased the amount of Ki-67 expression in M phase that increasing the correlation with telomerase activity, but decreased the amount of cyclin A expression in the same phase that presented a descending trend. The amounts of other cell cycle regulators expression were no different in whole cell cycles, but they changed the localization in cell cycles. So, they might be correlation with their function. In conclusion, strong telomerase activity in M phase of cell cycle was cell line specifically in HCC cell lines.
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