ArticleTranslational cancer research2026
Targeting chitinase-3-like protein 2 (CHI3L2) suppresses cell proliferation and migration in glioblastoma.
Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Glioblastoma (GBM), the most common and aggressive subtype of glioma, currently lacks effective therapeutic targets. This study aimed to elucidate the role of chitinase-3-like protein 2 (CHI3L2) and its underlying mechanism in GBM cell proliferation and migration. Methods: Gene Expression Profiling Interactive Analysis 2 (GEPIA2) and Chinese Glioma Genome Atlas (CGGA) databases were used to analyze the messenger RNA (mRNA) expression level of CHI3L2 and its prognostic significance in different grades of glioma patients. Western blotting was performed to determine the protein levels of CHI3L2 in different GBM cell lines. The efficiency of lentivirus-mediated CHI3L2 knockdown or overexpression was tested by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting in LN-229 and U251 cells. Cell proliferation was determined by cell counting kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays. Cell migration was detected by the wound healing assay. Cell cycle distribution was analyzed by flow cytometry. Protein levels of key cell cycle-related regulators (e.g., c-MYC, CDK2, CDK4) and migration-related regulators (e.g., E-cadherin, N-cadherin, MMP2, MMP9) were measured by Western blotting. Results: Integrated bioinformatics analysis demonstrated that high CHI3L2 expression was correlated with shortened overall survival (OS) and disease-free survival (DFS) in GBM patients. CHI3L2 knockdown significantly suppressed cell proliferation, G1/S transition, and cell migration in LN-229 and U251 cells; conversely, CHI3L2 overexpression facilitated these cellular processes. Furthermore, CHI3L2 knockdown markedly reduced the protein levels of c-MYC, CDK2, CDK4, N-cadherin, MMP2, and MMP9 but increased E-cadherin. Conclusions: Elevated CHI3L2 expression drives GBM cell proliferation and migration, suggesting that CHI3L2 is a promising therapeutic target for GBM.
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