YKL-40 promotes invasion and metastasis of bladder cancer by regulating epithelial mesenchymal transition

Abstract

Objective: This study aims to explore the relevance between YKL-40 and recurrence and progression of bladder cancer, and determine whether YKL-40 can be used as a potential target in patients with bladder cancer. Methods: We analyzed the invasion and metastasis ability of BIU-87, UMUC3, J82, T24, 5637 and immortalized human bladder epithelial cells SVHUC1 by Transwell method. The YKL-40 expression levels in cell lines were analyzed by Western blot and qPCR. Results: The increase of YKL-40 level, especially in tumour group, was related to tumour pathological stage and tumour invasion and metastasis. The cell lines with YKL-40 high expression had stronger invasion and metastasis ability. Overexpression of YKL-40 in SVHUC1 with the lowest YKL-40 expression can enhance the invasion and migration of cells. In T24 cells with YKL-40 high expression, transfection of shRNA plasmid targeting YKL-40 can down regulate the invasion and migration. The expression levels of N-cadherin and Vimentin in YKL-40 overexpressed SVHUC1 cells were increased, the E-cadherin expression was decreased, the Twist, Snail and Slug expression levels were increased, but they were opposite in T24 cells with down-regulation of YKL-40 expression. Conclusions: YKL-40 promoted the migration and invasion of bladder cancer cells by up regulating the EMT gene expression. The YKL-40 expression is closely related to the invasion and migration of bladder cancer.

Upregulation of YKL-40 Promotes Metastatic Phenotype and Correlates with Poor Prognosis and Therapy Response in Patients with Colorectal Cancer

“…In both cell lines, regardless of the genetic background, YKL-40 expression caused changes in CRC cell migration, invasion, and proliferation, three crucial characteristics of advanced tumors. The wound-healing assay showed that the expression level of YKL-40 is closely related to the migration rate of CRC cells, in agreement with what was observed in endothelial cells [ 53 ], glioblastoma [ 37 ], and prostate cancer cells [ 54 ]. The invasion assays revealed a determinant role of YKL-40 in promoting the invasion of CRC cells, thus implying an increase in metastatic potential, as observed in other tumors [ 31 ].…”

“…Hao et al concluded that YKL-40 promotes bladder cancer metastasis by regulating EMT genes such as E-cadherin, Twist, Snail, Slug, N-cadherin, and vimentin [ 63 ]. In our study, we also examined the same set of EMT-related markers, so we can assume that the glycoprotein plays a similar role in CRC.…”

Functional analysis of the short splicing variant encoded by CHI3L1/YKL-40 in glioblastoma

“…Functionally, the altered regulation of interferon signaling contributes to the immune evasion of glioma cells as well as the maintenance of glioblastoma stem cells ( 31 , 32 ). In addition, regulation of EMT by YKL-40 to promote tumor progression has been observed in many cancers, including GBM ( 33 – 36 ). Taken in the context of our transcriptome data, it is possible that both isoforms could generate glioma stem cells that favor microenvironments contributing to GBM aggressiveness, recurrence, and resistance to radiation and chemotherapy.…”

Emerging Biomarkers of Multiple Sclerosis in the Blood and the CSF: A Focus on Neurofilaments and Therapeutic Considerations

“…This is no surprise, as CHI3L1 was shown to bind to different extracellular matrix constituents and several other molecules regulating the processes mentioned above [ 130 , 135 , 136 ]. Altered levels of CHI3L1 are strongly associated with many malignant and non-malignant diseases and various neurodegenerative disorders, including MS [ 130 , 137 , 138 , 139 , 140 , 141 , 142 , 143 ]. Multiple factors (age, changes in the extracellular matrix, various cytokines and growth factors, stress, inflammation) have been identified that influence the production of CH3L1, many of which are also prominent factors in the pathogenesis of MS [ 130 ].…”