Analysis of ovarian tumourigenesis due to activators for histone deacetylases(HDACs) that are highly overexpressed in cancers

原癌基因Gankyrin在卵巢癌中过度表达。甘草蛋白加速了pRb蛋白的降解。Gankyrin抑制p16INK4a与CDK4的相互作用。甘草蛋白增强MDM2对P53蛋白的降解作用。Gankyrin抑制NFkappaB的活性，部分原因是SIRT1组蛋白脱乙酰酶重新聚集到NFkappaB蛋白上。HSCO基因在卵巢癌中过表达。HSCO通过HDAC1组蛋白脱乙酰酶向P53蛋白募集，从而抑制P53的活性。Gankyrin和HSCO激活HDAC的活性。这些增强的HDAC活性加速了癌细胞的生长，使其更具侵略性。这些激活的HDAC增强了肿瘤的侵袭和转移活性。烟酰胺抑制SIRT1活性。TSA(曲古抑素A)抑制HDAC1活性。这些HDAC抑制剂抑制癌细胞的生长、侵袭和转移。

Protooncogene Gankyrin is overexpressed in ovarian cancer. Gankyrin accelerates to degrade pRb protein. Gankyrin inhibits the interaction of p16INK4a with cdk4. Gankyrin enhances to degrade p53 protein by MDM2. Gankyrin suppresses the activity of NFkappaB, partly due to recruitment of SIRT1 histone deacetylase to NFkappaB protein. HSCO gene is overexpressed in ovarian cancer. HSCO inhibits the activity of p53 due to recruitment of HDAC1 histone deacetylase to p53 protein. Gankyrin and HSCO activate the activity of HDACs. These enhanced activities of HDACs accelerate to grow cancer cells more aggressively. The activities of invasion and metastasis are enhanced due to these activated HDACs. Nicotinamide suppresses SIRT1 activity. TSA(Trichostatin A) inhibits HDAC1 activity. These HDAC inhibitors suppress the growth, invasion, and metastasis of cancer cells.