Crosstalk between the CBM complex/NF-κB and MAPK/P27 signaling pathways of regulatory T cells contributes to the tumor microenvironment
Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-in...
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Published in | Frontiers in cell and developmental biology Vol. 10; p. 911811 |
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Abstract | Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1–BCL10–MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors. |
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AbstractList | Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1–BCL10–MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors. Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1-BCL10-MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors.Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1-BCL10-MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors. |
Author | Wang, Dongming Luo, Ying Qi, Tongbing Cui, Weitong Tian, Xuewen Ma, Xuan Wang, Qinglu Zhou, Yue |
AuthorAffiliation | 2 Key Laboratory of Biomedical Engineering and Technology of Shandong High School , Qilu Medical University , Zibo , China 4 Department of Pediatrics , People’s Hospital of Huantai , Zibo , China 3 Clinical Laboratory , Zibo Central Hospital , Zibo , China 1 College of Sport and Health, Shandong Sport University , Jinan , China |
AuthorAffiliation_xml | – name: 2 Key Laboratory of Biomedical Engineering and Technology of Shandong High School , Qilu Medical University , Zibo , China – name: 3 Clinical Laboratory , Zibo Central Hospital , Zibo , China – name: 4 Department of Pediatrics , People’s Hospital of Huantai , Zibo , China – name: 1 College of Sport and Health, Shandong Sport University , Jinan , China |
Author_xml | – sequence: 1 givenname: Tongbing surname: Qi fullname: Qi, Tongbing – sequence: 2 givenname: Ying surname: Luo fullname: Luo, Ying – sequence: 3 givenname: Weitong surname: Cui fullname: Cui, Weitong – sequence: 4 givenname: Yue surname: Zhou fullname: Zhou, Yue – sequence: 5 givenname: Xuan surname: Ma fullname: Ma, Xuan – sequence: 6 givenname: Dongming surname: Wang fullname: Wang, Dongming – sequence: 7 givenname: Xuewen surname: Tian fullname: Tian, Xuewen – sequence: 8 givenname: Qinglu surname: Wang fullname: Wang, Qinglu |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Reviewed by: Yunshan Wang, Shandong University, China Edited by: Shahrzad Jalali, Mayo Clinic, United States These authors have contributed equally to this work This article was submitted to Signaling, a section of the journal Frontiers in Cell and Developmental Biology |
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SubjectTerms | CARMA1 CBM signaling pathway Cell and Developmental Biology MAPK/P27 signaling pathway regulatory T cells tumor microenvironment |
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Title | Crosstalk between the CBM complex/NF-κB and MAPK/P27 signaling pathways of regulatory T cells contributes to the tumor microenvironment |
URI | https://www.proquest.com/docview/2699703287 https://pubmed.ncbi.nlm.nih.gov/PMC9343696 https://doaj.org/article/fff4b6ee87bb4286be031a0a57d1c4c8 |
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