scholarly journals MPPa-PDT suppresses breast tumor migration/invasion by inhibiting AKT-NF-κB-dependent MMP-9 expression via ROS

2019 ◽  
Author(s):  
Liyi Huang ◽  
Haidan Lin ◽  
Qing Chen ◽  
Lehua Yu ◽  
dingqun bai
Keyword(s):  
Breast Cancer ◽  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Actin Cytoskeleton ◽  
Breast Tumor ◽  
Tumor Metastasis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mcf 7

Abstract Abstract Background: Breast cancer is one of the most commonly diagnosed cancers in women, with high morbidity and mortality. Tumor metastasis is implicated in most breast cancer deaths; thus, inhibiting metastasis may provide a therapeutic direction for breast cancer. In the present study, pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) was used to inhibit metastasis in MCF-7 breast cancer cells. Methods: Uptake of MPPa was detected by fluorescence microscopy. Cell viability was evaluated by the Cell Counting Kit-8 (CCK-8). ROS generation was detected by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA). The migration of cells was assessed by wound healing assay, and invasion ability was assessed by Matrigel invasion assay. Levels of MMP2 and MMP9 were measured by PCR. Akt, phospho-Akt (Ser473), phospho-NF-κB p65 (Ser536) and NF-κB p65 were measured by western blotting. The F-actin cytoskeleton was observed by immunofluorescence. Lung tissue was visualized by hematoxylin and eosin staining. Results: Following MPPa-PDT, migration and invasion were decreased in the MCF-7 cells. MPPa-PDT downregulated the expression of MMP2 and MMP9, which are responsible for the initiation of metastasis. MPPa-PDT reduced the phosphorylation of Akt and NF-κB. MPPa-PDT also reduced and destroyed the F-actin cytoskeleton in MCF-7 cells. These effects were blocked by the reactive oxygen species scavenger NAC or the Akt activator SC79, while the PI3K inhibitor LY294002 or the Akt inhibitor triciribine enhanced these effects. Moreover, MPPa-PDT inhibited tumor metastasis and destroyed F-actin in vivo. Conclusion: Taken together, these results demonstrate that MPPa-PDT inhibits the metastasis of MCF-7 cells both in vitro and in vivo and may be involved in the Akt/NF-κB-dependent MMP-9 signaling pathway. Thus, MPPa-PDT may be a promising treatment to inhibit metastasis. Key words: photodynamic therapy, reactive oxygen species, breast tumor, migration, invasion

scholarly journals Rare-Earth-Doped Calcium Carbonate Exposed to X-ray Irradiation to Induce Reactive Oxygen Species for Tumor Treatment

2019 ◽  
Vol 20 (5) ◽  
pp. 1148 ◽  
Author(s):  
Chun-Chen Yang ◽  
Wei-Yun Wang ◽  
Feng-Huei Lin ◽  
Chun-Han Hou
Keyword(s):  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Tumor Growth ◽  
Light Source ◽  
Reactive Oxygen ◽  
Blood Analysis ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
X Ray

Conventional photodynamic therapy (PDT) is limited by its penetration depth due to the photosensitizer and light source. In this study, we developed X-ray induced photodynamic therapy that applied X-ray as the light source to activate Ce-doped CaCO3 (CaCO3:Ce) to generate an intracellular reactive oxygen species (ROS) for killing cancer cells. The A549 cell line was used as the in vitro and in vivo model to evaluate the efficacy of X-ray-induced CaCO3:Ce. The cell viability significantly decreased and cell cytotoxicity obviously increased with CaCO3:Ce exposure under X-ray irradiation, which is less harmful than radiotherapy in tumor treatment. CaCO3:Ce produced significant ROS under X-ray irradiation and promoted A549 cancer cell death. CaCO3:Ce can enhance the efficacy of X-ray induced PDT, and tumor growth was inhibited in vivo. The blood analysis and hematoxylin and eosin stain (H&E) stain fully supported the safety of the treatment. The mechanisms underlying ROS and CO2 generation by CaCO3:Ce activated by X-ray irradiation to induce cell toxicity, thereby inhibiting tumor growth, is discussed. These findings and advances are of great importance in providing a novel therapeutic approach as an alternative tumor treatment.

Synthesis and evaluation of new 5-aminolevulinic acid derivatives as prodrugs of protoporphyrin for photodynamic therapy

2017 ◽  
Vol 16 (11) ◽  
pp. 1623-1630 ◽  
Author(s):  
Wei Zhu ◽  
Ying-Hua Gao ◽  
Chun-Hong Song ◽  
Zhi-Bin Lu ◽  
Tabbisa Namulinda ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Aminolevulinic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Light Activation ◽  
S180 Cell

Upon light activation, 13a can induce the production of PpIX in vivo which produces ROS and other reactive oxygen species to lead to the apoptosis of S180 cell tumors.

scholarly journals The effective in vivo mitochondrial-targeting nanocarrier combined with a π-extended porphyrin-type photosensitizer

2021 ◽  
Author(s):  
Satrialdi . ◽  
Yuta Takano ◽  
Eri Hirata ◽  
Natsumi Ushijima ◽  
H. Harashima ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Photodynamic Therapy ◽  
Cancer Therapy ◽  
Molecular Oxygen ◽  
Photochemical Reaction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Targeting

A photochemical reaction mediated by light-activated molecules (photosensitizers) in photodynamic therapy (PDT) causes molecular oxygen to be converted into highly reactive oxygen species (ROS) that is beneficial for cancer therapy....

scholarly journals Reactive oxygen species modulate macrophage immunosuppressive phenotype through the up-regulation of PD-L1

2019 ◽  
Vol 116 (10) ◽  
pp. 4326-4335 ◽  
Author(s):  
Cecilia Roux ◽  
Soode Moghadas Jafari ◽  
Rahul Shinde ◽  
Gordon Duncan ◽  
David W. Cescon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Reactive Oxygen Species ◽  
Cytotoxic T Cells ◽  
Reactive Oxygen ◽  
Immune Checkpoint Blockade ◽  
Tumor Burden ◽  
Oxygen Species ◽  
Synthesis Inhibitor

The combination of immune checkpoint blockade with chemotherapy is currently under investigation as a promising strategy for the treatment of triple negative breast cancer (TNBC). Tumor-associated macrophages (TAMs) are the most prominent component of the breast cancer microenvironment because they influence tumor progression and the response to therapies. Here we show that macrophages acquire an immunosuppressive phenotype and increase the expression of programmed death ligand-1 (PD-L1) when treated with reactive oxygen species (ROS) inducers such as the glutathione synthesis inhibitor, buthionine sulphoximine (BSO), and paclitaxel. Mechanistically, these agents cause accumulation of ROS that in turn activate NF-κB signaling to promote PD-L1 transcription and the release of immunosuppressive chemokines. Systemic in vivo administration of paclitaxel promotes PD-L1 accumulation on the surface of TAMS in a mouse model of TNBC, consistent with in vitro results. Combinatorial treatment with paclitaxel and an anti-mouse PD-L1 blocking antibody significantly improved the therapeutic efficacy of paclitaxel by reducing tumor burden and increasing the number of tumor-associated cytotoxic T cells. Our results provide a strong rationale for the use of anti–PD-L1 blockade in the treatment of TNBC patients. Furthermore, interrogation of chemotherapy-induced PD-L1 expression in TAMs is warranted to define appropriate patient selection in the use of PD-L1 blockade.

scholarly journals Reactive Oxygen Species Generated by 17β-estradiol Play a Role in the Up-regulation of GPX4 Protein in MCF-7 Breast Cancer Cells

2009 ◽  
Vol 12 (3) ◽  
pp. 134 ◽  
Author(s):  
Sang-Han Lee ◽  
Hee Jeong Kim ◽  
Hyo Jin Kang ◽  
Yoon-Jin Lee ◽  
Hae-Seon Nam ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Reactive Oxygen Species ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
17Β Estradiol ◽  
Mcf 7
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