ArticleAnnals of medicine2021
YKL-40 promotes invasion and metastasis of bladder cancer by regulating epithelial mesenchymal transition.
Article in Annals of medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Effect of the miR‑26a/b‑5p‑STAT3‑YKL‑40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells.Oncology reports · 2026Article
- Differential contribution of TFE3 isoforms to cell motility and invasion.EMBO reports · 2026Article
- Targeting of YKL-40 as a Protumor in Personalized Medicine: A New Dimension in Disease Understanding.Current gene therapy · 2026Review
- Early Detection of Prostate Cancer Using Novel ELISA-Based Biomarkers: Insights into Inflammatory and Tumor-Specific Pathways.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Investigating the relationship between peripheral blood transferrin receptor protein and tumor cell ferroptosis, invasion, and metastasis in bladder cancer.Scientific reports · 2025Article
- YKL-40 inhibits melanoma progression and metastasis by inducing immune cell infiltration in a mouse model.Scientific reports · 2025Article
- Uncovering novel mechanisms of chitinase-3-like protein 1 in driving inflammation-associated cancers.Cancer cell international · 2024Review
- Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response.Cancer metastasis reviews · 2024Review
- Chitinase 3-like 1 expression associated with lymphatic metastasis and prognosis in urothelial carcinoma of the bladder.Clinical & translational immunology · 2024Article
- Chitinase 3-like-1 Expression in the Microenvironment Is Associated with Neutrophil Infiltration in Bladder Cancer.International journal of molecular sciences · 2023Article
- Article
- Alpha-2 Heremans Schmid Glycoprotein (AHSG) promotes the proliferation of bladder cancer cells by regulating the TGF-β signalling pathway.Bioengineered · 2022Article
- Emerging Biomarkers of Multiple Sclerosis in the Blood and the CSF: A Focus on Neurofilaments and Therapeutic Considerations.International journal of molecular sciences · 2022Review
- Functional analysis of the short splicing variant encoded by CHI3L1/YKL-40 in glioblastoma.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis 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.
methodsWe 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.
resultsThe 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.
conclusionsYKL-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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.