Cell Cycle Arrest Effects by Artemisia annua Linne in Hep3B Liver Cancer Cell
2015
Kim, E.J., Hannam University, Daejeon, Republic of Korea | Kim, G.T., Hannam University, Daejeon, Republic of Korea | Kim, B.M., Hannam University, Daejeon, Republic of Korea | Lim, E.G., Hannam University, Daejeon, Republic of Korea | Kim, S.Y., Department of BIONGENE, Seoul, Republic of Korea | Ha, S.H., Hannam University, Daejeon, Republic of Korea | Kim, Y.M., Hannam University, Daejeon, Republic of Korea | Yoo, J.G., Hannam University, Daejeon, Republic of Korea
Cells proliferate via repeating process that growth and division. This process is G1, S, G2 and M four phases consists. Monitoring the progression of the cell cycle is a specific step that to be a continuous process is repeated to adjust the start of the next step. At this time, this process is called a Checkpoint. Currently, there are three known checkpoints that G1-S phase, G2-M phase, and the M phase. In this study, we confirmed that cell cycle arrest effects by ethanol extracts of Artemisia annua Linne (AAE) in Hep3B liver cancer cells. AAE was regulated proteins which involved in cell cycle such as pAkt, pMDM2, p53, p21, pCDK2 (T14/Y15). AAE induced cell cycle arrest in G1 checkpoint through phosphorylation of CDK2. Akt and p53 upstream is inhibited by AAE and p53 activated by non-activated pMDM2, p53 inhibitor. Thereby, activated p53 is transcript to p21 and activated p21 protein is combined with Cyclin E-pCDK2 complex. Therefore, we confirmed that AAE-induced cell cycle arrest was occurred by p21-Cyclin E-pCDK2 complex by inhibition of pAkt signal. Because of this cell cycle can't pass to S phase from G1 phase.
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