CHI3L1 plays a role in cancer through enhanced production of pro-inflammatory/pro-tumorigenic and angiogenic factors

Libreros, Stephania; Garcia-Areas, Ramon; Iragavarapu-Charyulu, Vijaya

doi:10.1007/s12026-013-8459-y

Cited by 91 publications

(96 citation statements)

References 79 publications

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“…The most prominent cytokine/chemokine detected in the SCLC CTC supernatants CHI3L1 is also known as YKL-40 (86). CH3L1 pseudo-chitinase, which exhibits an inactivated enzymatic site but has retained chitin-binding activity, functions as regulatory factor of normal cell types, including macrophages (106). CHI3L1/YKL-40 has been described as soluble marker of invasive cancers with poor prognosis for a wide range of malignancies including lung cancer and, particularly, SCLC.…”

Section: Chi3l1 In Inflammation and Cancermentioning

confidence: 99%

“…Lung metastasis of melanoma and breast cancer cells was reduced after blocking ChI3L1 with antibodies or removing its regulator semaphorin 7a in experimental animals (98). Treatment with chitin microparticles inhibited tumor growth and angiogenesis at primary tumor sites but also reduced metastasis to the lung (106,111). CHI3L1 was also shown to bind the surface "Receptor for Advance Glycation End" Product (RAGE) which supports progression of solid tumors through promotion cell proliferation, migration and survival (112).…”

Section: Chi3l1 In Inflammation and Cancermentioning

confidence: 99%

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Circulating tumor cell interactions with macrophages: implications for biology and treatment

Hamilton¹,

Rath²

2017

Transl. Lung Cancer Res.

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CTCs. SCLC has an unfavorable prognosis due to rapid dissemination and early chemoresistant relapses. SCLC CTCs recruit macrophages and elicit secretion of various cytokines and the six CTC lines expresschitinase-3-like-1 (CHI3L1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP9) in abundance. CHI3L1 is cytokine/growth factor expressed in inflammation and cancer and found to be correlated to metastasis and a dismal prognosis. In conclusion, SCLC CTCs have acquired the essential means for aggressiveness and invasion in a tumor microenvironment specifically shaped by macrophages and inflammation.

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Section: Chi3l1 In Inflammation and Cancermentioning

confidence: 99%

Section: Chi3l1 In Inflammation and Cancermentioning

confidence: 99%

Circulating tumor cell interactions with macrophages: implications for biology and treatment

Hamilton¹,

Rath²

2017

Transl. Lung Cancer Res.

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“…In assessing the clinical significance of MMPs, such as MMP-9 in melanoma patients, Lugowska et al [15] found that serum concentrations of VEGF, MMP-2 and -9, and YKL-40/CHI3L1 were significantly higher in melanoma patients compared with the control group. YKL-40/CHI3L1 was one of the tumor-and host-derived factors that induced the expression of MMP-9 by macrophages [16,17].…”

Section: Tumor-associated Inflammationmentioning

confidence: 99%

“…TAMs contribute to tumor growth and metastasis by secreting MMPs that promote extracellular matrix remodeling; angiogenic factors that increase blood vessel formation; and cytokines, chemokines, and growth factors that enhance tumor growth [18,19]. Specifically, TAMs have been reported to produce VEGF, epidermal growth factor, basic fibroblast growth factor, platelet-derived growth factor, IL-6, MCP-1, CXCL18, CXCL12, and YKL-40/CHI3L1 [16,[20][21][22][23][24][25]. YKL-40/CHI3L1 induces the expression of MCP-1/CCL2 and IL-8/CXCL2, which are chemoattractants for monocytes/ macrophages and neutrophils [16].…”

Section: Tumor-associated Inflammationmentioning

confidence: 99%

“…Specifically, TAMs have been reported to produce VEGF, epidermal growth factor, basic fibroblast growth factor, platelet-derived growth factor, IL-6, MCP-1, CXCL18, CXCL12, and YKL-40/CHI3L1 [16,[20][21][22][23][24][25]. YKL-40/CHI3L1 induces the expression of MCP-1/CCL2 and IL-8/CXCL2, which are chemoattractants for monocytes/ macrophages and neutrophils [16]. All of these factors may serve as angiogenic molecules.…”

Section: Tumor-associated Inflammationmentioning

confidence: 99%

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YKL-40/CHI3L1 drives inflammation on the road of tumor progression

Libreros

Iragavarapu-Charyulu

2015

Journal of Leukocyte Biology

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Inflammation plays a vital role at different stages of tumor progression. The development of tumors is affected by inflammatory mediators produced by the tumor and the host. YKL-40/chitinase-3-like-1 protein is often upregulated in inflammation-associated diseases. With the use of chronic inflammatory disease systems, we describe the role of YKL-40/chitinase-3-like-1 protein in enhancing the inflammatory response and its implications in tumorigenesis. We also discuss how pre-existing inflammation enhances tumor growth and metastasis. In this mini-review, we highlight the effect of YKL-40/ chitinase-3-like-1 protein-associated inflammation in promoting tumor progression. J. Leukoc. Biol. 98: 931-936;

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Circulating monocytes from prostate cancer patients promote invasion and motility of epithelial cells

et al. 2018

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BackgroundRecruited myeloid cells are known to promote cancer initiation, malignant progression, metastasis, and resistance to therapy in the tumor niche. We tested the hypothesis that circulating blood monocytes from advanced prostate cancer (PCa) patients exhibit a protumor phenotype and directly influence the tumor microenvironment in response to tumor‐derived signals.MethodsBlood monocytes from advanced and stable PCa patients were cultured, and the conditioned media (CM) were collected and analyzed using standard invasion and wound closure assays to measure effects on invasion and motility of PCa tumor cells. We then identified the proteome profile of these monocytes using proteome array and ELISA.ResultsConditioned media from circulating monocytes in patients with metastatic prostate cancer (PCa‐M) increased invasion of epithelial PCa cells in vitro. Proteome Profiler Analysis revealed that monocyte‐derived CM from metastatic castration‐resistant (mCRPC) patients presented high levels of chitinase‐3‐like 1 (CHI3L1, YKL‐40) when compared to patients with stable disease (PCa‐N) and healthy control individuals (HC). The only described receptor for CHI3L1, interleukin‐13 receptor α2 (IL‐13Rα2), was significantly up‐regulated in the human metastatic PCa cell line, ARCaPM. Accordingly, we observed that the activation of IL‐13Rα2 from PCa‐M CM increased the invasiveness of ARCaPM cells while siRNA directed against this receptor significantly reduced invasiveness of these cells in the presence of CM from PCa‐M patients.ConclusionsThus, we show that circulating monocytes from metastatic PCa patients exert a tumor‐promoting role via the secretion of CHI3L1, and CHI3L1 demands further exploration as a possible therapeutic target in advanced PCa.

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CHI3L1 plays a role in cancer through enhanced production of pro-inflammatory/pro-tumorigenic and angiogenic factors

Cited by 91 publications

References 79 publications

Circulating tumor cell interactions with macrophages: implications for biology and treatment

Circulating tumor cell interactions with macrophages: implications for biology and treatment

YKL-40/CHI3L1 drives inflammation on the road of tumor progression

Circulating monocytes from prostate cancer patients promote invasion and motility of epithelial cells

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