Reversal of T-cell exhaustion: Mechanisms and synergistic approaches DOI
Yang Hu, Yaqi Zhang,

Fenfen Shi

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 138, P. 112571 - 112571

Published: June 28, 2024

Language: Английский

Mxene/Au@Co Bimetallic Enzyme Ec-Spr Microfluidic Sensing Platform for On-Chip in Situ Monitoring of H2o2 in Living Cells DOI
Yuanyuan Chen, Xiaoqing Jiang,

Zhongquan Song

et al.

Published: Jan. 1, 2025

Language: Английский

Citations

0

Cascade-enhanced based-polyoxometalates nanozyme for glutathione detection and tumor cell disruption DOI

Jianian Guo,

Hong Han, Hong Zhao

et al.

Talanta, Journal Year: 2025, Volume and Issue: 291, P. 127890 - 127890

Published: March 3, 2025

Language: Английский

Citations

0

Inflammation-targeted nanomedicine prevents tumor metastasis following photodynamic therapy by reversing epithelial-mesenchymal transition and ROS-mediated immunosuppression DOI Creative Commons
Zhengwei Song,

Quanwei Sun,

Wenshuo Yang

et al.

Journal of Nanobiotechnology, Journal Year: 2025, Volume and Issue: 23(1)

Published: April 4, 2025

Prolonging the duration of photodynamic therapy (PDT) enhances level reactive oxygen species (ROS), thereby facilitating tumor ablation. However, our findings indicated that excessive ROS not only induces epithelial-mesenchymal transition (EMT) but also creates an immunosuppressive microenvironment in tumor, triggering metastasis. We initially developed neutrophil membrane hybrid liposomes (NLs) can specifically target inflamed tissues following PDT. Then, we utilized NLs to encapsulate antioxidant nanozyme FeGA and antiplatelet drug Lysine Acetylsalicylate (LAS), resulting formulation NLASF. Experimental results demonstrated effectively scavenges ROS, reversing induced by prolonged Furthermore, incorporation LAS disrupts interaction between cells platelets, mitigating EMT inhibiting hematogenous In a breast cancer mouse model, observed treatment with NLASF led near-complete suppression lung metastasis Additionally, vivo application did result any blood toxicity or organ toxicity, highlighting its significant advantages over free drugs group. This study provides novel approach enhance efficacy PDT successfully suppress PDT-mediated

Language: Английский

Citations

0

A triple-cascade nanoreactor for potent anti-tumor chemodynamic and immunotherapy DOI
Yilu Zheng,

Yichao Du,

Hang Yin

et al.

Colloids and Surfaces B Biointerfaces, Journal Year: 2025, Volume and Issue: unknown, P. 114732 - 114732

Published: April 1, 2025

Language: Английский

Citations

0

A CuS/Ag/Pt@ICG/DOX nanoplatform with cascaded nanozyme catalysis for tumor microenvironment remodeling and synergistic photodynamic/photothermal/chemodynamic therapy DOI
Wenqi Zhu,

Dong Cheng,

Linsong Li

et al.

Colloids and Surfaces B Biointerfaces, Journal Year: 2025, Volume and Issue: unknown, P. 114743 - 114743

Published: April 1, 2025

Language: Английский

Citations

0

Macrophages in tumor cell migration and metastasis DOI Creative Commons

Madeline Friedman-DeLuca,

George S. Karagiannis,

John S. Condeelis

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 1, 2024

Tumor-associated macrophages (TAMs) are a phenotypically diverse, highly plastic population of cells in the tumor microenvironment (TME) that have long been known to promote cancer progression. In this review, we summarize TAM ontogeny and polarization, then explore how TAMs enhance cell migration through TME, thus facilitating metastasis. We also discuss chemotherapy host factors including diet, obesity, race, impact phenotype brief, induce epithelial-mesenchymal transition (EMT) cells, giving them migratory phenotype. They extracellular matrix (ECM) remodeling, allowing migrate more easily. provide chemotactic signals directional towards blood vessels, participate signaling cascade at vessel allows intravasate disseminate throughout body. Furthermore, while can repolarize an anti-tumor response, these cytotoxic drugs lead macrophage-mediated relapse Patient response may be dependent on patient-specific such as shown alter macrophage affect cancer-related outcomes. More research progression is needed refine treatment strategies for patients.

Language: Английский

Citations

3

The Impact of Atmospheric Cadmium Exposure on Colon Cancer and the Invasiveness of Stents within the Cancerous Colon DOI Open Access
Shuai Zhang,

Ruikang Li,

Jing Xu

et al.

Published: Jan. 8, 2024

Background: Inhalation exposure to carcinogenic metals like cadmium (Cd) is a significant global health concern linked various cancers. However, understanding their precise mechanism remains elusive. Methods: Using the colon cancer (CC) rat model and implanted intestinal stent, exposed them atomized oxygen nitrogen (O2/N2) gas containing Cd. Results: Atmospheric Cd intensified inflammation in CC cells, heightening nicotinamide adenine dinucleotide phosphate 1 (NOX1) activity, generating increased reactive species (ROS). This escalated ROS production triggered abnormal Wnt protein secretion, activating Wnt/β-catenin pathway, stimulating cell proliferation. No discernible body weight effect was seen mice, possibly due later-stage tumor gain, masking changes. facilitated restructuring migration later. Intestinal stents inhibited superoxide dismutase (SOD1) mice's tumors, with no clear effects on NOX1, SOD2, catalase (CAT) enzymes. Elevated levels didn't substantially impact might slow its imbalance. Stent implantation eased inflammation, reducing proliferation but induced discomfort rats, food intake weight. Conclusion: partially foster tumorigenesis via ROS-mediated pathway. The of invasive cancerous not significant.

Language: Английский

Citations

2

Emergency myelopoiesis in solid cancers DOI
Konstantinos Aliazis, Sasitorn Yenyuwadee, Ployploen Phikulsod

et al.

British Journal of Haematology, Journal Year: 2024, Volume and Issue: 205(3), P. 798 - 811

Published: July 23, 2024

Summary Cells of the innate and adaptive immune systems are progeny haematopoietic stem progenitor cells (HSPCs). During steady‐state myelopoiesis, HSPC undergo differentiation proliferation but called to respond directly acutely various signals that lead emergency including bone marrow ablation, infections, sterile inflammation. There is extensive evidence many solid tumours have potential secrete classical myelopoiesis‐promoting growth factors other products able mimic haematopoiesis, aberrantly re‐direct myeloid cell development into immunosuppressive with tumour promoting properties. Here, we summarize current literature regarding effects cancers on HSPCs function discuss how these might shape antitumour responses via a mechanism initiated at site distal from microenvironment.

Language: Английский

Citations

2

Comprehensive multi-omics analysis of the prognostic value and immune signature of NCF2 in pan-cancer and its relationship with acute myeloid leukemia DOI

Fangfang Zhong,

Yan Zeng,

Yuzhi Yan

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113364 - 113364

Published: Oct. 10, 2024

Language: Английский

Citations

2

Reactive oxygen species: Janus-faced molecules in the era of modern cancer therapy DOI Creative Commons

Aine O’Reilly,

Wenchao Zhao, Stina L. Wickström

et al.

Journal for ImmunoTherapy of Cancer, Journal Year: 2024, Volume and Issue: 12(12), P. e009409 - e009409

Published: Dec. 1, 2024

Oxidative stress, that is, an unbalanced increase in reactive oxygen species (ROS), contributes to tumor-induced immune suppression and limits the efficacy of immunotherapy. Cancer cells have inherently increased ROS production, intracellularly through metabolic perturbations extracellularly activation NADPH oxidases, which promotes cancer progression. Further production or impaired antioxidant systems, induced, for example, by chemotherapy radiotherapy, can preferentially kill over healthy cells. Inflammatory cell-derived mediate immunosuppressive effects myeloid-derived suppressor activated granulocytes, hampering antitumor effector such as T natural killer (NK) therapies modulating levels tumors may thus entirely different consequences when targeting versus Here we discuss possibility developing more efficient based on reduction-oxidation modulation, either monotherapies combination with Short-term, systemic administration antioxidants drugs blocking boost system act synergy However, prolonged use instead enhance tumor Alternatives are under development where gene-modified NK shielded ex vivo against harmful before infusion patients cancer.

Language: Английский

Citations

2