YKL-40/chitinase-3-like protein 1 is associated with poor prognosis and promotes cell growth and migration of cholangiocarcinoma

Thongsom, Sunisa; Chaocharoen, W.; Silsirivanit, Atit; Wongkham, Sopit; Sripa, Banchob; Choe, Han; Suginta, Wipa; Talabnin, Chutima

doi:10.1007/s13277-016-4838-z

Cited by 27 publications

(22 citation statements)

References 49 publications

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“…Previous studies have demonstrated that YKL-40 is associated with oncogenesis (8,10). Elevated levels of serum YKL-40 were reported to be associated with several types of cancer, such as ovarian, esophageal, breast, lung, liver and kidney cancer (11)(12)(13)(14)(15)(16).…”

Section: Discussionmentioning

confidence: 99%

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Potential suppressive effects of theophylline on human rectal cancer SW480 cells inï¿½vitro by inhibiting YKL-40 expression

Peng

Zeng

et al. 2018

Oncol Lett

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Abstract. Chitinase-3-like-1 protein (YKL-40), a member of the mammalian chitinase-like glycoproteins, serves a key role in the pathogenesis of rectal cancer. The present study examined the antitumor effect of theophylline, a pan-chitinase inhibitor, in rectal cancer in vitro and investigated the mechanism by which it acted. SW480 cell lines were treated with varying theophylline concentrations (10 -2 , 10 -3, 10 -4 and 10 -5 mol/l). An MTT assay was used to observe cell proliferation and identify the optimal theophylline concentration. Western blotting was used to analyze YKL-40 expression. The cell cycle distribution of SW480 cell lines treated with theophylline was measured by flow cytometry. The angiopoietin-2 expression level was measured by ELISA. The expression levels of YKL-40 were evidently decreased in theophylline-treated SW480 cell lines. The proliferation ofSW480 cells was inhibited following theophylline treatment, which was associated with G 1 phase cell cycle arrest and a decrease in the expression of angiopoietin-2. The mechanism of theophylline action may involve the downregulation of YKL-40 expression, arrest of the cell cycle at G 1 phase and inhibition of angiopoietin-2 expression. These results provide a rationale for the potential use of anti-YKL-40 and anti-angiogenic strategies in treating rectal cancer.

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Section: Discussionmentioning

confidence: 99%

“…YKL-40 serves a critical role in cellular proliferation, differentiation, angiogenesis, remodeling of the extracellular matrix and apoptosis (5)(6)(7)(8)(9), and the aforementioned processes are important for tumor growth and dissemination (10). Therefore, YKL-40 may represent a novel attractive therapeutic target.…”

Section: Introductionmentioning

confidence: 99%

Potential suppressive effects of theophylline on human rectal cancer SW480 cells inï¿½vitro by inhibiting YKL-40 expression

Peng

Zeng

et al. 2018

Oncol Lett

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“…20 YKL-40 is involved in the development of hepatic fibrosis, 13 and elevated serum YKL-40 levels, which are associated with poor prognosis, have been described in patients with breast cancer, colorectal cancer, cholangiocellular carcinoma, and pancreatic cancer. [21][22][23][24] Although high serum YKL-40 levels are also associated with poor prognosis in HCC patients who undergo hepatic resection, the majority of enrolled patients in that study had HBV-or HCV-related HCC, which has different characteristics than non-viral HCC. 25 Thus, the clinical significance of YKL-40 in the prognosis of non-viral HCC patients remains unclear.…”

Section: Introductionmentioning

confidence: 92%

“…YKL‐40, also known as chitinase 3‐like‐1 or HC‐gp39, was originally discovered as a secreted protein from a human osteosarcoma cell line, and is expressed in non‐malignant cells . YKL‐40 is involved in the development of hepatic fibrosis, and elevated serum YKL‐40 levels, which are associated with poor prognosis, have been described in patients with breast cancer, colorectal cancer, cholangiocellular carcinoma, and pancreatic cancer . Although high serum YKL‐40 levels are also associated with poor prognosis in HCC patients who undergo hepatic resection, the majority of enrolled patients in that study had HBV‐ or HCV‐related HCC, which has different characteristics than non‐viral HCC .…”

Section: Introductionmentioning

confidence: 99%

High serum interleukin‐34 level is a predictor of poor prognosis in patients with non‐viral hepatocellular carcinoma

Noda

Kawaguchi

Korenaga

et al. 2019

Hepatology Research

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Aims We aimed to investigate the impact of interleukin (IL)‐34 and YKL‐40, regulators of hepatic fibrosis and tumor growth, on the prognosis of patients with non‐viral hepatocellular carcinoma (HCC). Methods We enrolled 159 non‐viral HCC patients (age, 70.8 ± 8.5 years; female/male, 43/116). Of these, 86 patients were alive and 73 patients had died at the censor time point. Serum IL‐34 and YKL‐40 levels were quantified by enzyme‐linked immunosorbent assay. Patients were stratified by the median level of serum IL‐34 to examine its effect on survival. Multivariate analysis and random forest analysis were used to evaluate the impact of IL‐34 and YKL‐40 on the prognosis of non‐viral HCC patients. Results Interleukin‐34 (hazard ratio [HR] 1.30; 95% confidence interval [CI], 1.13–1.49; P ≤ 0.01), tumor size (HR 1.63; 95% CI, 1.37–1.94; P ≤ 0.01), and tumor number (HR 1.53; 95% CI, 1.25–1.87; P ≤ 0.01) were independent predictive factors for survival. Furthermore, the survival rates were significantly lower in the high IL‐34 group than in the low IL‐34 group (5‐year survival rates, 34.7% vs. 59.8%, respectively; P < 0.05). In the random forest analysis for survival, IL‐34 was the third‐highest ranking factor, following tumor size and number. In a stratification analysis, serum α‐fetoprotein level and Fibrosis‐4 index were independent positive risk factors for high serum IL‐34 level. YKL‐40 was not associated with prognosis in either the multivariate or random forest analysis. Conclusion Interleukin‐34 was an independent factor for survival of non‐viral HCC patients. Interleukin‐34 might be associated with prognosis through tumor and hepatic fibrosis factors.

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“…Importantly, within the tumoral area, CCA cells represent only minor contributors to YKL-40 production, which is primarily caused by infiltrating inflammatory cells, especially TAMs. Of further interest, exogenous YKL-40 stimulated CCA cell growth and migration, by triggering Akt and ERK1/2 activation[81]. …”

Section: Tumor-associated Macrophagesmentioning

confidence: 99%

Tumor reactive stroma in cholangiocarcinoma: The fuel behind cancer aggressiveness

Brivio

Cadamuro

Strazzabosco

et al. 2017

WJH

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Cholangiocarcinoma (CCA) is a highly aggressive epithelial malignancy still carrying a dismal prognosis, owing to early lymph node metastatic dissemination and striking resistance to conventional chemotherapy. Although mechanisms underpinning CCA progression are still a conundrum, it is now increasingly recognized that the desmoplastic microenvironment developing in conjunction with biliary carcinogenesis, recently renamed tumor reactive stroma (TRS), behaves as a paramount tumor-promoting driver. Indeed, once being recruited, activated and dangerously co-opted by neoplastic cells, the cellular components of the TRS (myofibroblasts, macrophages, endothelial cells and mesenchymal stem cells) continuously rekindle malignancy by secreting a huge variety of soluble factors (cyto/chemokines, growth factors, morphogens and proteinases). Furthermore, these factors are long-term stored within an abnormally remodeled extracellular matrix (ECM), which in turn can deleteriously mold cancer cell behavior. In this review, we will highlight evidence for the active role played by reactive stromal cells (as well as by the TRS-associated ECM) in CCA progression, including an overview of the most relevant TRS-derived signals possibly fueling CCA cell aggressiveness. Hopefully, a deeper knowledge of the paracrine communications reciprocally exchanged between cancer and stromal cells will steer the development of innovative, combinatorial therapies, which can finally hinder the progression of CCA, as well as of other cancer types with abundant TRS, such as pancreatic and breast carcinomas.

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YKL-40/chitinase-3-like protein 1 is associated with poor prognosis and promotes cell growth and migration of cholangiocarcinoma

Cited by 27 publications

References 49 publications

Potential suppressive effects of theophylline on human rectal cancer SW480 cells inï¿½vitro by inhibiting YKL-40 expression

Potential suppressive effects of theophylline on human rectal cancer SW480 cells inï¿½vitro by inhibiting YKL-40 expression

High serum interleukin‐34 level is a predictor of poor prognosis in patients with non‐viral hepatocellular carcinoma

Tumor reactive stroma in cholangiocarcinoma: The fuel behind cancer aggressiveness

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