ROS-responsive nanomedicine: Towards targeting the breast tumor microenvironment

2020 ◽  
Vol 28 ◽  
Author(s):  
RamaRao Malla ◽  
Mohammad Amjad Kamal
Keyword(s):  
Reactive Oxygen Species ◽  
Gene Therapy ◽  
Drug Resistance ◽  
Molecular Imaging ◽  
Tumor Microenvironment ◽  
Immune Cells ◽  
Breast Tumor ◽  
Imaging Techniques ◽  
Oxygen Species ◽  
Massive Accumulation

: The breast tumor microenvironment (TME) promotes drug resistance through an elaborated interaction of TME components mediated by reactive oxygen species (ROS). Despite a massive accumulation of data concerning the targeting the ROS, but little is known about the ROS-responsive nanomedicine for targeting breast TME. This review submits the ROS landscape in breast TME, including ROS biology, ROS mediated carcinogenesis, reprogramming of stromal and immune cells of TME. We also discussed ROS-based precision strategies for imaging TME, including molecular imaging techniques with advanced probes, multiplexed methods, and multi-omic profiling strategies. ROS-responsive nanomedicine also describes various therapies, such as chemo-dynamic, photodynamic, photothermal, sono-dynamic, immune, and gene therapy for BC. We expound ROS-responsive primary delivery systems for chemotherapeutics, phytochemicals, and immunotherapeutics. This review also presents recent updates on nano-theranostics for simultaneous diagnosis and treatment of BCs. We assume that review on this advancing field will be beneficial to the development of ROS-based nanotheranostics for BC.

Reactive oxygen species (ROS): critical roles in breast tumor microenvironment

2021 ◽  
pp. 103285
Author(s):  
RamaRao Malla ◽  
Nagalakshmi Surepalli ◽  
Batoul Farran ◽  
Sanjay V. Malhotra ◽  
Ganji Purnachandra Nagaraju
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Microenvironment ◽  
Breast Tumor ◽  
Reactive Oxygen ◽  
Oxygen Species

The Tumor Microenvironment: Characterization, Redox Considerations, and Novel Approaches for Reactive Oxygen Species-Targeted Gene Therapy

2013 ◽  
Vol 19 (8) ◽  
pp. 854-895 ◽  
Author(s):  
Lucia Laura Policastro ◽  
Irene Laura Ibañez ◽  
Cintia Notcovich ◽  
Hebe Alicia Duran ◽  
Osvaldo Luis Podhajcer
Keyword(s):  
Reactive Oxygen Species ◽  
Gene Therapy ◽  
Tumor Microenvironment ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Novel Approaches ◽  
Targeted Gene Therapy

scholarly journals Targeted production of reactive oxygen species in mitochondria to overcome cancer drug resistance

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Hai Wang ◽  
Zan Gao ◽  
Xuanyou Liu ◽  
Pranay Agarwal ◽  
Shuting Zhao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Drug Resistance ◽  
Reactive Oxygen ◽  
Cancer Drug ◽  
Oxygen Species ◽  
Cancer Drug Resistance

scholarly journals Staphylococcal DNA Repair Is Required for Infection

mBio ◽  
2020 ◽  
Vol 11 (6) ◽  
Author(s):  
Kam Pou Ha ◽  
Rebecca S. Clarke ◽  
Gyu-Lee Kim ◽  
Jane L. Brittan ◽  
Jessica E. Rowley ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Staphylococcus Aureus ◽  
Human Blood ◽  
Immune Cells ◽  
Double Strand Breaks ◽  
Oxygen Species ◽  
Dna Double Strand Breaks ◽  
Gram Positive ◽  
Content Type ◽  
Strand Breaks

ABSTRACT To cause infection, Staphylococcus aureus must withstand damage caused by host immune defenses. However, the mechanisms by which staphylococcal DNA is damaged and repaired during infection are poorly understood. Using a panel of transposon mutants, we identified the rexBA operon as being important for the survival of Staphylococcus aureus in whole human blood. Mutants lacking rexB were also attenuated for virulence in murine models of both systemic and skin infections. We then demonstrated that RexAB is a member of the AddAB family of helicase/nuclease complexes responsible for initiating the repair of DNA double-strand breaks. Using a fluorescent reporter system, we were able to show that neutrophils cause staphylococcal DNA double-strand breaks through reactive oxygen species (ROS) generated by the respiratory burst, which are repaired by RexAB, leading to the induction of the mutagenic SOS response. We found that RexAB homologues in Enterococcus faecalis and Streptococcus gordonii also promoted the survival of these pathogens in human blood, suggesting that DNA double-strand break repair is required for Gram-positive bacteria to survive in host tissues. Together, these data demonstrate that DNA is a target of host immune cells, leading to double-strand breaks, and that the repair of this damage by an AddAB-family enzyme enables the survival of Gram-positive pathogens during infection. IMPORTANCE To cause infection, bacteria must survive attack by the host immune system. For many bacteria, including the major human pathogen Staphylococcus aureus, the greatest threat is posed by neutrophils. These immune cells ingest the invading organisms and try to kill them with a cocktail of chemicals that includes reactive oxygen species (ROS). The ability of S. aureus to survive this attack is crucial for the progression of infection. However, it was not clear how the ROS damaged S. aureus and how the bacterium repaired this damage. In this work, we show that ROS cause breaks in the staphylococcal DNA, which must be repaired by a two-protein complex known as RexAB; otherwise, the bacterium is killed, and it cannot sustain infection. This provides information on the type of damage that neutrophils cause S. aureus and the mechanism by which this damage is repaired, enabling infection.

scholarly journals Tumor-Specific Reactive Oxygen Species Accelerators Improve Chimeric Antigen Receptor T Cell Therapy in B Cell Malignancies

2019 ◽  
Vol 20 (10) ◽  
pp. 2469 ◽  
Author(s):  
Hyeon Joo Yoo ◽  
Yibin Liu ◽  
Lei Wang ◽  
Maria-Luisa Schubert ◽  
Jean-Marc Hoffmann ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
T Cell ◽  
Tumor Microenvironment ◽  
Chimeric Antigen Receptor ◽  
Antigen Receptor ◽  
Reactive Oxygen ◽  
Treatment Resistance ◽  
Lymphocytic Leukemia ◽  
Oxygen Species ◽  
T Cell Therapy

Chimeric antigen receptor T cell (CART) therapy is currently one of the most promising treatment approaches in cancer immunotherapy. However, the immunosuppressive nature of the tumor microenvironment, in particular increased reactive oxygen species (ROS) levels, provides considerable limitations. In this study, we aimed to exploit increased ROS levels in the tumor microenvironment with prodrugs of ROS accelerators, which are specifically activated in cancer cells. Upon activation, ROS accelerators induce further generation of ROS. This leads to an accumulation of ROS in tumor cells. We hypothesized that the latter cells will be more susceptible to CARTs. CD19-specific CARTs were generated with a CD19.CAR.CD28.CD137zeta third-generation retroviral vector. Cytotoxicity was determined by chromium-51 release assay. Influence of the ROS accelerators on viability and phenotype of CARTs was determined by flow cytometry. The combination of CARTs with the ROS accelerator PipFcB significantly increased their cytotoxicity in the Burkitt lymphoma cell lines Raji and Daudi, as well as primary chronic lymphocytic leukemia cells. Exposure of CARTs to PipFcB for 48 h did not influence T cell exhaustion, viability, or T cell subpopulations. In summary, the combination of CARTs with ROS accelerators may improve adoptive immunotherapy and help to overcome tumor microenvironment-mediated treatment resistance.

scholarly journals Ultrasound-induced reactive oxygen species generation and mitochondria-specific damage by sonodynamic agent/metal ion-doped mesoporous silica

RSC Advances ◽  
2019 ◽  
Vol 9 (68) ◽  
pp. 39924-39931 ◽  
Author(s):  
Kecan Lin ◽  
Ziguo Lin ◽  
Yujie Li ◽  
Youshi Zheng ◽  
Da Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Microenvironment ◽  
Cancer Therapy ◽  
Mesoporous Silica ◽  
Metal Ion ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species

Herein, we design tumor microenvironment specific active nano sono-chemodynamic agent for synergistic photodynamic–chemodynamic cancer therapy.

scholarly journals STIM-Orai Channels and Reactive Oxygen Species in the Tumor Microenvironment

Cancers ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 457 ◽  
Author(s):  
Janina Frisch ◽  
Adrian Angenendt ◽  
Markus Hoth ◽  
Leticia Prates Roma ◽  
Annette Lis
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Microenvironment ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Blood Vessels ◽  
Cancer Cell ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Soluble Factors ◽  
Orai Channels

The tumor microenvironment (TME) is shaped by cancer and noncancerous cells, the extracellular matrix, soluble factors, and blood vessels. Interactions between the cells, matrix, soluble factors, and blood vessels generate this complex heterogeneous microenvironment. The TME may be metabolically beneficial or unbeneficial for tumor growth, it may favor or not favor a productive immune response against tumor cells, or it may even favor conditions suited to hijacking the immune system for benefitting tumor growth. Soluble factors relevant for TME include oxygen, reactive oxygen species (ROS), ATP, Ca2+, H+, growth factors, or cytokines. Ca2+ plays a prominent role in the TME because its concentration is directly linked to cancer cell proliferation, apoptosis, or migration but also to immune cell function. Stromal-interaction molecules (STIM)-activated Orai channels are major Ca2+ entry channels in cancer cells and immune cells, they are upregulated in many tumors, and they are strongly regulated by ROS. Thus, STIM and Orai are interesting candidates to regulate cancer cell fate in the TME. In this review, we summarize the current knowledge about the function of ROS and STIM/Orai in cancer cells; discuss their interdependencies; and propose new hypotheses how TME, ROS, and Orai channels influence each other.

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