Ying Kong1, Xiaogai Qi, Peisong Bai, Kejun Nan. 1. Department of Oncology, First Affiliated Hospital, Medical School, Xi'an Jiaotong University, China. koyin@126.com
Abstract
OBJECTIVE: To investigate the role of the cell cycle-related novel gene CDK2-associated, culin clomain 1(CACUL1) in tumor cell apopotosis and explore the relationship between CACUL1 and apoptosis regulation. METHODS: We induced the cell cycle arrest by ultraviolet radiation and chemotherapeutic drugs and then studied the expression of CACUL1 in cell DNA damage state. Meanwhile, Western blotting, Northern blotting and other methods were applied to detect the expression of the CACUL1 at both protein and mRNA levels and analyze their relationships with p53 in p53 wild-type and knock-out colorectal cancer cells. RESULTS: The CACUL1 was proved related to the regulation of apoptosis. In the case of DNA damage induced by ultraviolet radiation and chemotherapeutic drugs, the expression of CACUL1 protein peaked at 2 h, and with time went by, the expression of CACUL1 gradually decreased. The increase of CACUL1 expression was independent of p53. Northern blotting revealed that the increased expression of CACUL1 was post-transcriptional regulation. It was also found that the high expression of CACUL1 inhibited cell apoptosis induced by ultraviolet radiation and chemotherapeutic drugs. CONCLUSION: The role of CACUL1 in cell apoptosis is to help cells cross the G1/S checkpoints in a posttranscriptional regulation of p53-independent manner, thus facilitating cell survival.
OBJECTIVE: To investigate the role of the cell cycle-related novel gene CDK2-associated, culin clomain 1(CACUL1) in tumor cell apopotosis and explore the relationship between CACUL1 and apoptosis regulation. METHODS: We induced the cell cycle arrest by ultraviolet radiation and chemotherapeutic drugs and then studied the expression of CACUL1 in cell DNA damage state. Meanwhile, Western blotting, Northern blotting and other methods were applied to detect the expression of the CACUL1 at both protein and mRNA levels and analyze their relationships with p53 in p53 wild-type and knock-out colorectal cancer cells. RESULTS: The CACUL1 was proved related to the regulation of apoptosis. In the case of DNA damage induced by ultraviolet radiation and chemotherapeutic drugs, the expression of CACUL1 protein peaked at 2 h, and with time went by, the expression of CACUL1 gradually decreased. The increase of CACUL1 expression was independent of p53. Northern blotting revealed that the increased expression of CACUL1 was post-transcriptional regulation. It was also found that the high expression of CACUL1 inhibited cell apoptosis induced by ultraviolet radiation and chemotherapeutic drugs. CONCLUSION: The role of CACUL1 in cell apoptosis is to help cells cross the G1/S checkpoints in a posttranscriptional regulation of p53-independent manner, thus facilitating cell survival.