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      Blood Stasis Syndrome Accelerates the Growth and Metastasis of Breast Cancer by Promoting Hypoxia and Immunosuppressive Microenvironment in Mice

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          Abstract

          Blood stasis syndromes (BSSs) are closely related to the occurrence and development of tumors, although the mechanism is still unclear. This study was aimed at exploring the effect and mechanism underlying different BSSs on tumor growth and metastasis. We established four BSS mouse models bred with breast cancer: qi deficiency and blood stasis (QDBS), cold coagulation blood stasis (CCBS), heat toxin and blood stasis (HTBS), and qi stagnation and blood stasis (QSBS). The results showed that microcirculation in the lower limb, abdominal wall, and tumor in situ decreased by varying degrees in the BSS groups. In addition, BSS promoted tumor growth and lung metastasis. The ratio of regulatory T cells in the tumor microenvironment was downregulated. Moreover, hypoxia-inducible factor 1- α, Wnt1, β-catenin, vascular endothelial growth factor, and Cyclin D1 levels increased in the tumors of BSS mice. In conclusion, BSS not only promoted the formation of a hypoxic and immunosuppressive microenvironment but also promoted the neovascularization.

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          Inflammation and Cancer: Triggers, Mechanisms, and Consequences

          Florian Greten, Sergei I. Grivennikov (2019)
          Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells as well as surrounding stromal and inflammatory cells engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression and metastasis. We discuss how tumor promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis or tissue repair, and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatio-temporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for the further development of anti-cancer therapies. Grivennikov and Greten review the mechanisms underlying the initiation of pro-tumorigenic inflammatory responses, how these evolve throughout the different stages of tumor development and the plasticity of the cells within the tumor microenvironment.
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            Regulatory T cells in cancer immunosuppression — implications for anticancer therapy

            Yosuke Togashi, Kohei Shitara, Hiroyoshi Nishikawa (2019)
            Regulatory T (Treg) cells, an immunosuppressive subset of CD4+ T cells characterized by the expression of the master transcription factor forkhead box protein P3 (FOXP3), are a component of the immune system with essential roles in maintaining self-tolerance. In addition, Treg cells can suppress anticancer immunity, thereby hindering protective immunosurveillance of neoplasia and hampering effective antitumour immune responses in tumour-bearing hosts, thus promoting tumour development and progression. Identification of the factors that are specifically expressed in Treg cells and/or that influence Treg cell homeostasis and function is important to understanding cancer pathogenesis and to identifying therapeutic targets. Immune-checkpoint inhibitors (ICIs) have provided a paradigm shift in the treatment of cancer. Most immune-checkpoint molecules are expressed in Treg cells, but the effects of ICIs on Treg cells, and thus the contributions of these cells to treatment responses, remain unclear. Notably, evidence indicates that ICIs targeting programmed cell death 1 (PD-1) might enhance the immunosuppressive function of Treg cells, whereas cytotoxic T lymphocyte antigen 4 (CTLA-4) inhibitors might deplete these cells. Thus, although manipulation of Treg cells is a promising anticancer therapeutic strategy, approaches to controlling these cells require further research. Herein, we discuss novel insights into the roles of Treg cells in cancer, which can hopefully be used to develop Treg cell-targeted therapies and facilitate immune precision medicine.
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              Inflammation and tumor progression: signaling pathways and targeted intervention

              Huakan Zhao, Lei Wu, Guifang Yan … (2021)
              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 tumor progression and treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells (DCs) and antigen presentation, leading to anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers and activators of transcription (JAK-STAT), toll-like receptor (TLR) pathways, cGAS/STING, and mitogen-activated protein kinase (MAPK); inflammatory factors, including cytokines (e.g., interleukin (IL), interferon (IFN), and tumor necrosis factor (TNF)-α), chemokines (e.g., C-C motif chemokine ligands (CCLs) and C-X-C motif chemokine ligands (CXCLs)), growth factors (e.g., vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β), and inflammasome; as well as inflammatory metabolites including prostaglandins, leukotrienes, thromboxane, and specialized proresolving mediators (SPM), have been identified as pivotal regulators of the initiation and resolution of inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, and SPM have been developed to specifically modulate inflammation in cancer therapy, with some of these factors already undergoing clinical trials. Herein, we discuss the initiation and resolution of inflammation, the crosstalk between tumor development and inflammatory processes. We also highlight potential targets for harnessing inflammation in the treatment of cancer.
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                Author and article information

                Contributors
                Bing Ji:
                ORCID: https://orcid.org/0000-0003-0456-3321
                Qiyang Shou:
                ORCID: https://orcid.org/0000-0003-1615-5309
                Huiying Fu:
                ORCID: https://orcid.org/0000-0002-1782-5258
                Journal
                Journal ID (nlm-ta): J Immunol Res
                Journal ID (iso-abbrev): J Immunol Res
                Journal ID (publisher-id): jir
                Title: Journal of Immunology Research
                Publisher: Hindawi
                ISSN (Print): 2314-8861
                ISSN (Electronic): 2314-7156
                Publication date Collection: 2022
                Publication date (Electronic): 7 June 2022
                Volume: 2022
                Electronic Location Identifier: 7222638
                Affiliations
                1Second Clinical Medical School, Zhejiang Provincial Key Laboratory of Sexual Function of Integrated Traditional Chinese and Western Medicine, Zhejiang Chinese Medical University, Hangzhou 310053, China
                2Huzhou Hospital of Traditional Chinese Medicine, Affiliated Zhejiang Chinese Medicine University, Huzhou, 313003, China
                3Nanxun People's Hospital, Huzhou 313003, China
                4School of Pharmacy, Zhejiang Chinese Medical University, Hangzhou 310005, China
                5School of Basic Medicine, Zhejiang Chinese Medical University, Hangzhou 310005, China
                Author notes

                Academic Editor: Kai Wang

                Author information
                https://orcid.org/0000-0003-0456-3321
                https://orcid.org/0000-0003-1615-5309
                https://orcid.org/0000-0002-1782-5258
                Article
                DOI: 10.1155/2022/7222638
                PMC ID: 9197668
                SO-VID: db5a71e2-3179-4cfc-96fd-662f6d3ec7e2
                Copyright © Copyright © 2022 Lu Jin et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 December 2021
                Date revision received : 15 March 2022
                Date accepted : 17 March 2022
                Funding
                Funded by: Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents
                Funded by: Department of Education of Zhejiang Province
                Award ID: Y202146149
                Funded by: National Natural Science Foundation of China
                Award ID: 82174026
                Award ID: 81873047
                Award ID: 81673645
                Funded by: Science and Technology Program of Huzhou City
                Award ID: 2018GY05
                Funded by: China Postdoctoral Science Foundation
                Award ID: 2018M630693
                Funded by: Zhejiang Provincial Open Fund for Key Universities with Advantages and Characteristics
                Award ID: ZYXZD2019002
                Funded by: Natural Science Foundation of Zhejiang Province
                Award ID: LY19H270001
                Categories
                Subject: Research Article

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