Dinuclear phosphorescent rhenium(i) complexes as potential anticancer and photodynamic therapy agents

Ruthenium polypyridyl complexes inhibit cancer growth by targeting TrxR and promote the intracellular ROS generation, ultimately triggering mitochondria-mediated cell apoptosis.

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The effects of photodynamic therapy on leukemia cells mediated by KillerRed, a genetically encoded fluorescent protein photosensitizer

BMC Cancer ◽

10.1186/s12885-019-6124-0 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 1

Author(s):

Meng Yuan ◽

Chengcheng Liu ◽

Jiao Li ◽

Wenpeng Ma ◽

Xiaozhuo Yu ◽

...

Keyword(s):

Flow Cytometry ◽

Photodynamic Therapy ◽

Western Blotting ◽

Cell Apoptosis ◽

Fluorescent Protein ◽

Laser Scanning Microscopy ◽

Myelogenous Leukemia ◽

Leukemia Cells ◽

Acute Monocytic Leukemia ◽

Monocytic Leukemia

Abstract Background Leukemia is a cancer of blood and bone marrow cells, causing about 300,000 deaths worldwide. Photodynamic therapy (PDT) is a promising alternative for the treatment of malignant tumors. KillerRed is a genetically encoded red fluorescent protein photosensitizer (PS). In this study, we aimed to investigate the effects of KillerRed-mediated PDT on chronic myelogenous leukemia K562 cells, acute monocytic leukemia NB4 cells, and acute monocytic leukemia THP1 cells. Methods KillerRed was expressed in Escherichia coli cells, purified by Q-Sepharose column, and confirmed by western-blotting. The PDT effect on cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8). Cell apoptosis was determined by PE Annexin V/7-AAD staining and flow cytometry. The distribution of KillerRed in leukemia cells was detected by confocal laser scanning microscopy (CLSM) and western-blotting. The ROS generation was measured by flow cytometry. Results Pure KillerRed was obtained with a yield of about 37 mg per liter of bacterial cells. KillerRed photodynamic inactivated the leukemia cells in a concentration-dependent manner, but exhibited no obvious dark toxicity. PDT mediated by KillerRed could also induce apoptotic response (mainly early apoptosis) in the three cell lines. The CLSM imaging indicated that KillerRed was distributed within the cytoplasm and nuclei of leukemia cells, causing damages to the cytoplasm and leaving the nuclear envelope intact during light irradiation. KillerRed distributed both in the cytosol and nuclei was confirmed by western blotting, and ROS significantly increased in PDT treated cells compared to the cells treated with KillerRed alone. Conclusions Our studies demonstrated that KillerRed-mediated PDT could effectively inactivate K562, NB4, and THP1 leukemia cells and trigger cell apoptosis, and it has potential to be used individually or complementally, in the treatment of leukemia.

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Iron-based nanoparticles for MR imaging-guided ferroptosis in combination with photodynamic therapy to enhance cancer treatment

Nanoscale ◽

10.1039/d0nr08757b ◽

2021 ◽

Vol 13 (9) ◽

pp. 4855-4870

Author(s):

Qifang Chen ◽

Xianbin Ma ◽

Li Xie ◽

Wenjie Chen ◽

Zhigang Xu ◽

...

Keyword(s):

Photodynamic Therapy ◽

Mr Imaging ◽

Cancer Treatment ◽

Antitumor Effects ◽

Therapy Strategy ◽

Intracellular Ros ◽

Iron Based

MR imaging-guided a synergistic ferroptosis-photodynamic therapy strategy can enhance antitumor effects by accumulating intracellular ROS through the utilization of iron-based nanoparticles.

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Two macrocyclic polyamines as modulators of metal-mediated Aβ40aggregation

Integrative Biology ◽

10.1039/c5ib00064e ◽

2015 ◽

Vol 7 (6) ◽

pp. 655-662 ◽

Cited By ~ 14

Author(s):

Yanfei Yang ◽

Tingting Chen ◽

Shajun Zhu ◽

Xuefang Gu ◽

Xueping Jia ◽

...

Keyword(s):

Cell Apoptosis ◽

Intracellular Ros ◽

Macrocyclic Polyamines ◽

L1 And L2

L1 and L2 can inhibit the metal-induced Aβ40aggregation, attenuate neurotoxicity, suppress the intracellular ROS and protect against cell apoptosis.

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Aloe-Emodin-Mediated Photodynamic Therapy Induces Apoptosis in Basal Cell Carcinoma Cells via Activation of ERK/JNK Signaling Pathway

International Journal of Photoenergy ◽

10.1155/2021/6935269 ◽

2021 ◽

Vol 2021 ◽

pp. 1-10

Author(s):

Woodvine Otieno Odhiambo ◽

Songmei Geng ◽

Xiaopeng Wang ◽

Xiaodong Chen ◽

Mengting Qin ◽

...

Keyword(s):

Photodynamic Therapy ◽

T Cell ◽

Basal Cell Carcinoma ◽

Cell Carcinoma ◽

Basal Cell ◽

Cell Apoptosis ◽

Cost Effective ◽

Dependent Manner ◽

T Cell Apoptosis ◽

Aloe Emodin

Basal cell carcinoma (BCC) is the most prevalent epidermal cancerous neoplasm. Previous studies have reported the noninvasive, cost-effective, and localized photodynamic therapy (PDT) approach to BCC treatment. This study investigated the photodynamic effects of aloe-emodin (AE), a natural anthraquinone photosensitizer (PS), on proliferation and apoptosis of BCC TE 354.T cell line. To evaluate the effects of AE-mediated PDT, we used various concentrations of AE (0, 2.5, 5, and 10 μM) and white light energy (0, 12, 24, and 36 J/cm2). CCK-8 assay was used to analyse cell viability following AE-mediated PDT. The cell death rate and reactive oxygen species (ROS) were assessed by flow cytometry. Western blotting was used to determine the effects of AE-mediated PDT on the apoptotic proteins, Akt, and MAPK pathways. AE-mediated PDT inhibited tumorigenic cell proliferation, consequently enhancing apoptosis in AE and PDT concentration and dose-dependent manner, respectively. Significantly increased TE 354.T cell apoptosis and intracellular ROS production were both observed after AE-mediated PDT. Following the AE-mediated PDT, cytochrome and antitumor p53 were elevated; however expression of Bcl-2 was significantly decreased. Significant caspase 3 elevation post-AE-mediated PDT suggested intrinsically driven apoptosis. Additionally, AE-mediated PDT significantly suppressed NF-κB, Akt, and ERK pathways while JNK expression was significantly increased. AE-mediated PDT induced TE 354.T cell apoptosis through the intracellular generation of ROS. Akt, ERK, and JNK all play various roles in ensuring successful TE 354.T tumor cell apoptosis.

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Development of erythrosine-based photodynamic therapy with a targeted drug delivery system to induce HepG2 cell apoptosis in vitro

Biochemical Engineering Journal ◽

10.1016/j.bej.2021.108267 ◽

2021 ◽

pp. 108267

Author(s):

Bo-Chuan Hsieh ◽

Yen-Hsuan Ni ◽

Gu-Ming Zhang ◽

Yu-Chuan Chiu ◽

Yung-Te Hou

Keyword(s):

Drug Delivery ◽

Photodynamic Therapy ◽

Drug Delivery System ◽

Hepg2 Cell ◽

Delivery System ◽

Targeted Drug Delivery ◽

Cell Apoptosis ◽

Targeted Drug ◽

Targeted Drug Delivery System

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Regulation of intracellular Ca2+ in the cytotoxic response to photodynamic therapy with a chlorin-based photosensitizer

Journal of Porphyrins and Phthalocyanines ◽

10.1142/s1088424609001066 ◽

2009 ◽

Vol 13 (07) ◽

pp. 811-817 ◽

Cited By ~ 6

Author(s):

Je-Ok Yoo ◽

Chang-Hee Lee ◽

Byeong-Moon Hwang ◽

Woo Jin Kim ◽

Young-Myeong Kim ◽

...

Keyword(s):

Photodynamic Therapy ◽

Gastric Adenocarcinoma ◽

Irradiation Time ◽

Brefeldin A ◽

Ruthenium Red ◽

Dependent Manner ◽

Adenocarcinoma Cells ◽

Intracellular Ros ◽

Intracellular Ca ◽

Human Gastric Adenocarcinoma

We investigated regulation of intracellular Ca2+ induced by photodynamic therapy (PDT) with a new chlorin-based photosensitizer, DH-II-24, in human gastric adenocarcinoma cells. DH-II-24-mediated PDT induced necrotic cell death according to post-irradiation time, and produced intracellular reactive oxygen species (ROS) in an irradiation time-dependent manner. PDT also increased intracellular Ca2+ , and this Ca2+ elevation was largely inhibited by BAPTA-AM but not by EGTA. BAPTA-AM inhibited the ROS production by PDT, whereas NAC and Trolox had no effect on the PDT-induced Ca2+ response. In the presence of EGTA, pre-incubation with thapsigargin, Gly-Phe-β-naphthylamide or brefeldin A had no significant effect on the PDT-induced elevation in intracellular Ca2+ . However, ruthenium red affected the initial and late Ca2+ responses to PDT. Thus, DH-II-24-mediated PDT produces intracellular ROS via elevation in intracellular Ca2+ , contributed, at least in part, by mitochondria, which results in necrotic death of the human gastric adenocarcinoma cells.

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