Role of YKL-40 in the Angiogenesis, Radioresistance, and Progression of Glioblastoma

Francescone, Ralph; Scully, Steve; Faibish, Michael; Taylor, Sherry L.; Oh, Dennis; Moral, Luis; Yan, Wei; Bentley, Brooke; Shao, Rong

doi:10.1074/jbc.m110.212514

Cited by 227 publications

(256 citation statements)

References 48 publications

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“…Preclinical studies and experimental models using glioma cells indicate a role of CHI3L1 in tumor dissemination and drug resistance (110). The ability of CHI3L1 to bind heparan sulfates allows its interaction with cell surface proteoglycan syndecan-1, resulting in VEGF production and enhanced angiogenesis in glioblastoma (110).…”

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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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%

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

Hamilton¹,

Rath²

2017

Transl. Lung Cancer Res.

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“…Despite increasing knowledge about the effects of radiation on biochemical pathways, the exact mechanisms of intrinsic radioresistance remain unclear. To date, it has been reported that a number of key cellular features appear to play a role in the development of intrinsic radioresistance, including overexpression of DNA repair proteins (8), modifications of signaling pathways (9), angiogenesis (10) and the presence of cancer stem cells (11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs and Their Impact on Radiotherapy for Cancer

et al. 2016

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“…[15][16][17] In many of these disorders, YKL-40 correlates with disease activity and its expression is believed to reflect distinct pathways in disease pathogenesis. [18][19][20] However, to date, the expression and biology of Brp-39/YKL-40 in the kidney, its roles in the pathogenesis of acute or other forms of kidney injury, and its utility as a biomarker for renal diseases have not been investigated.…”

mentioning

confidence: 99%

Chitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function

Schmidt

Hall

Kale

et al. 2013

Journal of the American Society of Nephrology

106

102

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Kidney hypoperfusion during episodes of systemic hypotension or after surgical procurement for transplantation can lead to tubular cell death via necrosis and apoptosis, which trigger a series of responses that promote repair. The factors that contribute to the repair phase after kidney injury are not well understood. Using a urine proteomic screen in mice, we identified the macrophage-secreted chitinase-like protein Brp-39, the murine protein product of the chitinase 3-like 1 gene, as a critical component of this reparative response that serves to limit tubular cell apoptotic death via activation of Akt, improving animal survival after kidney ischemia/reperfusion. Examination of graded times of renal ischemia revealed a direct correlation between the degree of kidney injury and both Chi3l1/Brp-39 expression in the kidney and its levels in the urine. In samples collected from patients undergoing deceased-donor kidney transplantation, we found higher levels of the orthologous human protein, YKL-40, in urine and blood from allografts subjected to sufficient peri-transplant ischemia to cause delayed graft function than from allografts with slow or immediate graft function. Urinary levels of YKL-40 obtained within hours of transplant predicted the need for subsequent dialysis in these patients. In summary, these data suggest that Brp-39/YKL-40 is a sensor of the degree of injury, a critical mediator of the reparative response, and a possible biomarker to identify patients at greatest risk of sustained renal failure after transplantation.

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Role of YKL-40 in the Angiogenesis, Radioresistance, and Progression of Glioblastoma

Cited by 227 publications

References 48 publications

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

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

MicroRNAs and Their Impact on Radiotherapy for Cancer

Chitinase-Like Protein Brp-39/YKL-40 Modulates the Renal Response to Ischemic Injury and Predicts Delayed Allograft Function

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