scholarly journals IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway

2009 ◽  
Vol 206 (7) ◽  
pp. 1457-1464 ◽  
Author(s):  
Lin Wang ◽  
Tangsheng Yi ◽  
Marcin Kortylewski ◽  
Drew M. Pardoll ◽  
Defu Zeng ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Stromal Cells ◽  
Signal Transducer ◽  
Direct Effects ◽  
Th17 Response ◽  
Stat3 Signaling ◽  
Promote Tumor Growth ◽  
Stat3 Signaling Pathway ◽  
Ifn Γ

Although the Th17 subset and its signature cytokine, interleukin (IL)-17A (IL-17), are implicated in certain autoimmune diseases, their role in cancer remains to be further explored. IL-17 has been shown to be elevated in several types of cancer, but how it might contribute to tumor growth is still unclear. We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17−/− mice but drastically accelerated in IFN-γ−/− mice, contributed to by elevated intratumoral IL-17, indicating a role of IL-17 in promoting tumor growth. Adoptive transfer studies and analysis of the tumor microenvironment suggest that CD4+ T cells are the predominant source of IL-17. Enhancement of tumor growth by IL-17 involves direct effects on tumor cells and tumor-associated stromal cells, which bear IL-17 receptors. IL-17 induces IL-6 production, which in turn activates oncogenic signal transducer and activator of transcription (Stat) 3, up-regulating prosurvival and proangiogenic genes. The Th17 response can thus promote tumor growth, in part via an IL-6–Stat3 pathway.

IL-17 can promote tumor growth through an IL-6–Stat3 signaling pathway

2009 ◽  
Vol 186 (1) ◽  
pp. i2-i2
Author(s):  
Lin Wang ◽  
Tangsheng Yi ◽  
Marcin Kortylewski ◽  
Drew M. Pardoll ◽  
Defu Zeng ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Signaling Pathway ◽  
Stat3 Signaling ◽  
Promote Tumor Growth ◽  
Stat3 Signaling Pathway

scholarly journals Regulatory T cells promote glioma cell stemness through TGF-β–NF-κB–IL6–STAT3 signaling

2021 ◽  
Author(s):  
Shasha Liu ◽  
Chaoqi Zhang ◽  
Boqiao Wang ◽  
Huanyu Zhang ◽  
Guohui Qin ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Tumor Growth ◽  
Xenograft Model ◽  
Malignant Growth ◽  
Cancer Stemness ◽  
The Core ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Tumorigenic Potential

AbstractGlioma stem cells (GSCs) contribute to the malignant growth of glioma, but little is known about the interaction between GSCs and tumor microenvironment. Here, we found that intense infiltration of regulatory T cells (Tregs) facilitated the qualities of GSCs through TGF-β secretion that helped coordinately tumor growth. Mechanistic investigations indicated that TGF-β acted on cancer cells to induce the core cancer stem cell-related genes CD133, SOX2, NESTIN, MUSASHI1 and ALDH1A expression and spheres formation via NF-κB–IL6–STAT3 signaling pathway, resulting in the increased cancer stemness and tumorigenic potential. Furthermore, Tregs promoted glioma tumor growth, and this effect could be abrogated with blockade of IL6 receptor by tocilizumab which also demonstrated certain level of therapeutic efficacy in xenograft model. Additionally, expression levels of CD133, IL6 and TGF-β were found to serve as prognosis markers of glioma patients. Collectively, our findings reveal a new immune-associated mechanism underlying Tregs-induced GSCs. Moreover, efforts to target this network may be an effective strategy for treating glioma.

Abstract 536: Mesenchymal stromal cells promote tumor growth both in vitro and in vivo

2010 ◽  
Author(s):  
Kazuhiro Suzuki ◽  
Makoto Origuchi ◽  
Masahiko Kanehira ◽  
Ruowen Sun ◽  
Takenori Takahata ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Promote Tumor Growth

scholarly journals Exploring the key communicator role of exosomes in cancer microenvironment through proteomics

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
HuiSu Kim ◽  
Dong Wook Kim ◽  
Je-Yoel Cho
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Diagnosis ◽  
Stromal Cells ◽  
Cancer Biology ◽  
Immune Surveillance ◽  
Cancer Microenvironment ◽  
Promote Tumor Growth ◽  
Therapeutic Tools ◽  
Intercellular Communications

ABSTRACT There have been many attempts to fully understand the mechanism of cancer behavior. Yet, how cancers develop and metastasize still remain elusive. Emerging concepts of cancer biology in recent years have focused on the communication of cancer with its microenvironment, since cancer cannot grow and live alone. Cancer needs to communicate with other cells for survival, and thus they secrete various messengers, including exosomes that contain many proteins, miRNAs, mRNAs, etc., for construction of the tumor microenvironment. Moreover, these intercellular communications between cancer and its microenvironment, including stromal cells or distant cells, can promote tumor growth, metastasis, and escape from immune surveillance. In this review, we summarized the role of proteins in the exosome as communicators between cancer and its microenvironment. Consequently, we present cancer specific exosome proteins and their unique roles in the interaction between cancer and its microenvironment. Clinically, these exosomes might provide useful biomarkers for cancer diagnosis and therapeutic tools for cancer treatment.

scholarly journals Epstein-Barr Virus-Induced Gene 3 (EBI3) Blocking Leads to Induce Antitumor Cytotoxic T Lymphocyte Response and Suppress Tumor Growth in Colorectal Cancer by Bidirectional Reciprocal-Regulation STAT3 Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yanfang Liang ◽  
Qianqian Chen ◽  
Wenjing Du ◽  
Can Chen ◽  
Feifei Li ◽  
...  
Keyword(s):  
Tumor Growth ◽  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Reciprocal Regulation ◽  
Barr Virus ◽  
Cell Responses ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Epstein Barr

Epstein-Barr virus-induced gene 3 (EBI3) is a member of the interleukin-12 (IL-12) family structural subunit and can form a heterodimer with IL-27p28 and IL-12p35 subunit to build IL-27 and IL-35, respectively. However, IL-27 stimulates whereas IL-35 inhibits antitumor T cell responses. To date, little is known about the role of EBI3 in tumor microenvironment. In this study, firstly we assessed EBI3, IL-27p28, IL-12p35, gp130, and p-STAT3 expression with clinicopathological parameters of colorectal cancer (CRC) tissues; then we evaluated the antitumor T cell responses and tumor growth with a EBI3 blocking peptide. We found that elevated EBI3 may be associated with IL-12p35, gp130, and p-STAT3 to promote CRC progression. EBI3 blocking peptide promoted antitumor cytotoxic T lymphocyte (CTL) response by inducing Granzyme B, IFN-γproduction, and p-STAT3 expression and inhibited CRC cell proliferation and tumor growth to associate with suppressing gp130 and p-STAT3 expression. Taken together, these results suggest that EBI3 may mediate a bidirectional reciprocal-regulation STAT3 signaling pathway to assist the tumor escape immune surveillance in CRC.

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