Apoptosis induced by (di-isopropyloxyphoryl-Trp)2-Lys-OCH3 in K562 and HeLa cells

Journal of biosciences

Zhen-Hua Xie¹  Shi-Ying Liu¹  Yu-Yang Jiang1¹  Feng Liu¹  Ping Xu²  Guo-Ping Cai³ 

[1] The Key Laboratory of Chemical Biology, Guangdong Province, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen 518055, China$$;College of Bioengineering, Henan University of Technology, Zhengzhou 450052, China$$;Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, China$$

关键词: Apoptosis;    cell cycle;    HeLa;    K562;    N-phosphoryl dipeptide methyl ester;   

DOI  :  

来源: Indian Academy of Sciences

【 摘 要 】

According to the method used in our laboratory, our group synthesized (DIPP-Trp)2-Lys-OCH3. It inhibited the proliferation of K562 and HeLa cells in a dose- and time-dependent manner with an IC50 of 15.12 and 42.23 𝜇M, respectively. (DIPP-Trp)2-Lys-OCH3 induced a dose-dependent increase of the G2/M cell population in K562 cells, and S cell population in HeLa cells; the sub-G0 population increased dramatically in both cell lines as seen by PI staining experiments using a FACS Calibur Flow cytometer (BeckmanCoulter, USA). Phosphatidylserine could significantly translocate to the surface of the membrane in (DIPP-Trp)2-Lys-OCH3-treated K562 and HeLa cells. The increase of an early apoptotic population was observed in a dose-dependent manner by both annexin-FITC and PI staining. It was concluded that (DIPP-Trp)2-Lys-OCH3 not only induced cells to enter into apoptosis, but also affected the progress of the cell cycle. It may have arrested the K562 and HeLa cells in the G2/M, S phases, respectively. The apoptotic pathway was pulsed at this point, resulting in the treated cells entering into programmed cell death. (DIPP-Trp)2-Lys-OCH3 is a potential anticancer drug that intervenes in the signalling pathway.

【 授权许可】

Unknown