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Updated: Aug 17, 2026
An In Vitro Approach to Photodynamic Therapy
Published on: August 17, 2018
ZnPcS2P2-based photodynamic therapy induces mitochondria-dependent apoptosis in K562 cells
Hui-Fang Huang1, Yuan-Zhong Chen, Yong Wu
1Fujian Institute of Hematology, Union Hospital, Fujian Medical University, Fuzhou 350001, China.
Abstract:
Mitochondria play a key role in the regulation of apoptosis induced by numerous antitumor chemotherapeutic and other toxic agents. Photodynamic therapy (PDT) exerts significant cellular killing efficacy through either an apoptotic or necrotic cell death pathway. This study investigated the mechanism underlying the killing effects of a novel amphipathic photosensitizer [di-sulfonated di-phthalimidomethyl phthalocyanine zinc (ZnPcS2P2)]-mediated photodynamic therapy (ZnPcS2P2-PDT) on K562 cells. Apoptosis was evident in the post-PDT cells through the TdT-mediated dUTP nick end labeling (TUNEL) method and DNA fragmentation assay. After ZnPcS2P2-PDT, K562 cells underwent mitochondria-dependent apoptosis as evidenced by the release of cytochrome c from mitochondria into cytosol, accompanied by mitochondrial membrane potential (deltapsim) reduction, indicating the opening of the mitochondrial permeability transition pore (PTP). The activities of protease from the caspase family and caspase-3 were also significantly elevated. Furthermore, ZnPcS2P2-PDT down-regulated the expression of chimaeric Bcr-Abl oncoprotein, which is the molecular hallmark of chronic myelogenous leukemia (CML).
Insights
This study shows that novel photosensitizer-mediated photodynamic therapy (PDT) induces cancer cell death. Specifically, ZnPcS2P2-PDT triggers mitochondria-dependent apoptosis in K562 cells, a key mechanism in cancer treatment.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Mitochondria are crucial regulators of apoptosis, a programmed cell death pathway.
- Photodynamic therapy (PDT) is an effective cancer treatment modality that can induce apoptosis or necrosis.
- Chronic myelogenous leukemia (CML) is characterized by the Bcr-Abl oncoprotein.
Purpose of the Study:
- To investigate the cell death mechanisms of a novel photosensitizer, ZnPcS2P2-mediated photodynamic therapy (ZnPcS2P2-PDT), on K562 cells.
- To elucidate the role of mitochondria in ZnPcS2P2-PDT-induced cell death.
- To determine the effect of ZnPcS2P2-PDT on the expression of the Bcr-Abl oncoprotein.
Main Methods:
- K562 cells were treated with ZnPcS2P2-PDT.
- Apoptosis was assessed using the TUNEL method and DNA fragmentation assays.
- Mitochondrial changes, including cytochrome c release and mitochondrial membrane potential (ΔΨm) reduction, were measured.
- Caspase activity assays were performed.
- Western blotting was used to analyze Bcr-Abl oncoprotein expression.
Main Results:
- ZnPcS2P2-PDT induced apoptosis in K562 cells, confirmed by TUNEL assay and DNA fragmentation.
- Mitochondria-dependent apoptosis was observed, characterized by cytochrome c release and mitochondrial membrane potential dissipation, indicating PTP opening.
- Activities of caspases, including caspase-3, were significantly increased.
- ZnPcS2P2-PDT led to the down-regulation of the Bcr-Abl oncoprotein.
Conclusions:
- ZnPcS2P2-PDT effectively induces mitochondria-dependent apoptosis in K562 cells.
- The observed apoptosis involves the release of cytochrome c, PTP opening, and caspase activation.
- ZnPcS2P2-PDT exhibits potential as a therapeutic strategy by targeting CML cells and down-regulating Bcr-Abl.
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