Inflammation and tumor progression: signaling pathways and targeted intervention

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: July 12, 2021

Abstract Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates progression treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation dendritic cells (DCs) antigen presentation, leading anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers activators transcription (JAK-STAT), toll-like receptor (TLR) cGAS/STING, mitogen-activated protein kinase (MAPK); factors, including cytokines (e.g., interleukin (IL), interferon (IFN), necrosis (TNF)-α), chemokines C-C motif chemokine ligands (CCLs) C-X-C (CXCLs)), growth factors vascular endothelial (VEGF), transforming (TGF)-β), inflammasome; well metabolites prostaglandins, leukotrienes, thromboxane, specialized proresolving mediators (SPM), have been identified pivotal regulators initiation resolution inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, SPM developed specifically modulate in cancer therapy, with some these already undergoing clinical trials. Herein, we discuss crosstalk between processes. We also highlight potential targets for harnessing cancer.

Language: Английский

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Nanotechnology for Multimodal Synergistic Cancer Therapy

Chemical Reviews, Journal Year: 2017, Volume and Issue: 117(22), P. 13566 - 13638

Published: Oct. 19, 2017

The complexity, diversity, and heterogeneity of tumors seriously undermine the therapeutic potential treatment. Therefore, current trend in clinical research has gradually shifted from a focus on monotherapy to combination therapy for enhanced treatment efficacy. More importantly, cooperative enhancement interactions between several types contribute naissance multimodal synergistic therapy, which results remarkable superadditive (namely "1 + 1 > 2") effects, stronger than any single or their theoretical combination. In this review, state-of-the-art studies concerning recent advances nanotechnology-mediated will be systematically discussed, with an emphasis construction multifunctional nanomaterials realizing bimodal trimodal as well intensive exploration underlying mechanisms explaining significant improvements outcome. Furthermore, featured applications overcoming tumor multidrug resistance, hypoxia, metastasis also discussed detail, may provide new ways efficient regression even elimination drug resistant, hypoxic solid, distant metastatic tumors. Finally, some design tips outlook future development provided, highlighting key scientific issues technical challenges requiring remediation accelerate translation.

Language: Английский

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Targeting macrophages: therapeutic approaches in cancer

Nature Reviews Drug Discovery, Journal Year: 2018, Volume and Issue: 17(12), P. 887 - 904

Published: Oct. 26, 2018

Language: Английский

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Predictive biomarkers for checkpoint inhibitor-based immunotherapy

The Lancet Oncology, Journal Year: 2016, Volume and Issue: 17(12), P. e542 - e551

Published: Nov. 30, 2016

Language: Английский

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NK Cells Stimulate Recruitment of cDC1 into the Tumor Microenvironment Promoting Cancer Immune Control

Cell, Journal Year: 2018, Volume and Issue: 172(5), P. 1022 - 1037.e14

Published: Feb. 1, 2018

Conventional type 1 dendritic cells (cDC1) are critical for antitumor immunity, and their abundance within tumors is associated with immune-mediated rejection the success of immunotherapy. Here, we show that cDC1 accumulation in mouse often depends on natural killer (NK) produce chemoattractants CCL5 XCL1. Similarly, human cancers, intratumoral CCL5, XCL1, XCL2 transcripts closely correlate gene signatures both NK increased overall patient survival. Notably, tumor production prostaglandin E2 (PGE2) leads to evasion cell-cDC1 axis part by impairing cell viability chemokine production, as well causing downregulation receptor expression cDC1. Our findings reveal a cellular molecular checkpoint recruitment targeted tumor-derived PGE2 immune could be exploited cancer therapy.

Language: Английский

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Immunotherapy in colorectal cancer: rationale, challenges and potential

Nature Reviews Gastroenterology & Hepatology, Journal Year: 2019, Volume and Issue: 16(6), P. 361 - 375

Published: March 18, 2019

Language: Английский

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Oncolytic viruses: a new class of immunotherapy drugs

Nature Reviews Drug Discovery, Journal Year: 2015, Volume and Issue: 14(9), P. 642 - 662

Published: Sept. 1, 2015

Language: Английский

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NRF2 and the Hallmarks of Cancer

Cancer Cell, Journal Year: 2018, Volume and Issue: 34(1), P. 21 - 43

Published: May 3, 2018

Language: Английский

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New insights into cancer immunoediting and its three component phases—elimination, equilibrium and escape

Current Opinion in Immunology, Journal Year: 2014, Volume and Issue: 27, P. 16 - 25

Published: Feb. 14, 2014

Language: Английский

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Comprehensive review of targeted therapy for colorectal cancer

Signal Transduction and Targeted Therapy, Journal Year: 2020, Volume and Issue: 5(1)

Published: March 20, 2020

Abstract Colorectal cancer (CRC) is among the most lethal and prevalent malignancies in world was responsible for nearly 881,000 cancer-related deaths 2018. Surgery chemotherapy have long been first choices patients. However, prognosis of CRC has never satisfying, especially patients with metastatic lesions. Targeted therapy a new optional approach that successfully prolonged overall survival Following successes anti-EGFR (epidermal growth factor receptor) agent cetuximab anti-angiogenesis bevacizumab, agents blocking different critical pathways as well immune checkpoints are emerging at an unprecedented rate. Guidelines worldwide currently updating recommended targeted drugs on basis increasing number high-quality clinical trials. This review provides overview existing CRC-targeted their underlying mechanisms, discussion limitations future trends.

Language: Английский

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