[Inducement effect of (DIPP-L-Trp)2-L-Lys-OCH3 on apoptosis of K562 cells through mitochondrial-dependent pathway]
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Feng Liu1, Yu-Yang Jiang, Shi-Ying Liu
1Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, 100084, P. R. China.
Background & Objective:
Phosphorylation of protein and peptide plays an important role in life activity. Some phosphoryl peptides are found to have activities to inhibit proliferation of tumor cells, but the involved mechanisms are unclear. This study was designed to investigate cell apoptosis induced by (O,O-diisopropyl phosphoryl-L-tryptophan)(2)-L-lysine methyl ester [(DIPP-L-Trp)(2)-L-Lys-OCH(3)], and its mechanism in K562 cells.
Methods:
K562 cells were double stained by AnnexinV-FITC and propidium iodide (PI) to detect (DIPP-L-Trp)(2)-L-Lys-OCH(3)-induced apoptosis by flow cytometry (FCM). After treatment of different concentrations of (DIPP-L-Trp)(2)-L-Lys-OCH(3), K562 cells were stained by rhodamine123 and PI to detect changes in membrane potential (Delta Psi m), or stained by 2',7'-dichlorofluorescein diacetate (DCFH-DA) to detect reactive oxygen species (ROS) of mitochondrial by FCM.
Results:
When treated with 50 microg/ml of (DIPP-L-Trp)(2)-L-Lys-OCH(3) for 24 h, apoptosis rate of K562 cells was 61.9%, Delta Psi m was decreased in 93.6% of K562 cells,and ROS production was decreased. Both Delta Psi m and ROS production in K562 cells mitochondria were decreased with the increasing concentration and extending treatment time of (DIPP-L-Trp)(2)-L-Lys-OCH(3).
Conclusion:
(DIPP-L-Trp) (2)-L-Lys-OCH(2) could induce apoptosis in K562 cells, which might relate with down-regulation of mitochondrial Delta Psi m and reduction of ROS production.
Insights
This study shows that (O,O-diisopropyl phosphoryl-L-tryptophan)(2)-L-lysine methyl ester induces apoptosis in K562 cancer cells. The mechanism involves reduced mitochondrial membrane potential and decreased reactive oxygen species production.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Context:
- Protein and peptide phosphorylation is vital for cellular functions.
- Certain phosphorylated peptides exhibit anti-tumor properties, but their mechanisms remain unclear.
- Investigating novel compounds for cancer therapy is crucial.
Purpose:
- To investigate the mechanism of apoptosis induced by (O,O-diisopropyl phosphoryl-L-tryptophan)(2)-L-lysine methyl ester [(DIPP-L-Trp)(2)-L-Lys-OCH(3)] in K562 cells.
- To determine the role of mitochondrial membrane potential (Delta Psi m) and reactive oxygen species (ROS) in this process.
Summary:
- Treatment of K562 cells with (DIPP-L-Trp)(2)-L-Lys-OCH(3) resulted in a significant increase in apoptosis (61.9% at 50 microg/ml for 24 h).
- The compound induced a decrease in mitochondrial membrane potential (Delta Psi m) in 93.6% of cells.
- Both Delta Psi m and ROS production were dose- and time-dependently reduced by (DIPP-L-Trp)(2)-L-Lys-OCH(3).
Impact:
- This research elucidates a potential mechanism for the anti-cancer activity of (DIPP-L-Trp)(2)-L-Lys-OCH(3).
- Findings suggest that targeting mitochondrial function and ROS levels could be a viable strategy in cancer treatment.
- Provides a foundation for further investigation into phosphopeptide-based cancer therapeutics.
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