CAJ | 학술논문

蛋白磷酸酶Cdc25C能够使有丝分裂激酶CDK1/cyclin B去磷酸化,从而促进细胞周期的进程.已经在一些肿瘤细胞中检测到Cdc25C的过量表达,这使得Cde25C成为肿瘤治疗中的潜在靶标.通过随机筛选,发现了八个CAe25C的天然新抑制剂(1-8),其IC50值在1.66～75.07umol/L之间.肿瘤细胞毒试验结果表明,其中四个化合物(化合物3,4,5,7)对十种肿瘤细胞株显示一定的细胞毒活性,其IC50值皆小于10ug/ml.
단백린산매Cdc25C능구사유사분렬격매CDK1/cyclin B거린산화,종이촉진세포주기적진정.이경재일사종류세포중검측도Cdc25C적과량표체,저사득Cde25C성위종류치료중적잠재파표.통과수궤사선,발현료팔개CAe25C적천연신억제제(1-8),기IC50치재1.66～75.07umol/L지간.종류세포독시험결과표명,기중사개화합물(화합물3,4,5,7)대십충종류세포주현시일정적세포독활성,기IC50치개소우10ug/ml.
Protein phosphatase Cdc25C dephosphorylates the mitotic kinase CDK1/cyclin B, and then triggers the cell cycle progression. Overexpression of Cdc25C is detected in some cancer cells, which made it to be a potential target for anti-cancerdrugs. Through Cd25C assay, compounds 1-8 were found to be new natural inhibitors against Cdc25C with iC50s of 1.66-75.07μmol/L.Moreover,3,4,5and 7exhibited cytotoxicities on a panel of ten cancer cell lies with IC50 s below 10μg/mL.