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Updated: Apr 14, 2026
Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection
Published on: June 23, 2023
Targeting chitinase-3-like protein 2 (CHI3L2) suppresses cell proliferation and migration in glioblastoma
Zhihong Liu1,2, Dihui Chen3, Sijia Liao3
1School of Clinical Medicine, Guizhou Medical University, Guiyang, China.
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.
Insights
High chitinase-3-like protein 2 (CHI3L2) expression promotes glioblastoma growth and spread. Reducing CHI3L2 levels inhibits cancer cell proliferation and migration, identifying CHI3L2 as a potential therapeutic target for glioblastoma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioblastoma (GBM) is an aggressive brain cancer with limited treatment options.
- Chitinase-3-like protein 2 (CHI3L2) is implicated in cancer progression.
- The precise role of CHI3L2 in GBM remains to be fully elucidated.
Purpose of the Study:
- To investigate the role of CHI3L2 in glioblastoma cell proliferation and migration.
- To explore the underlying molecular mechanisms of CHI3L2 action in GBM.
- To assess the prognostic significance of CHI3L2 in glioma patients.
Main Methods:
- Bioinformatic analysis of GBM patient data (GEPIA2, CGGA) for CHI3L2 expression and survival correlation.
- In vitro studies using GBM cell lines (LN-229, U251) with CHI3L2 knockdown or overexpression.
- Assessment of cell proliferation (CCK-8, EdU), migration (wound healing), cell cycle (flow cytometry), and protein levels of key regulators (Western blotting).
Main Results:
- High CHI3L2 expression is linked to poorer overall survival and disease-free survival in GBM patients.
- CHI3L2 knockdown suppressed GBM cell proliferation, G1/S phase transition, and migration.
- CHI3L2 overexpression enhanced these cellular processes.
- CHI3L2 affects the expression of key proteins involved in cell cycle regulation (c-MYC, CDK2, CDK4) and cell migration (E-cadherin, N-cadherin, MMP2, MMP9).
Conclusions:
- Elevated CHI3L2 expression drives glioblastoma cell proliferation and migration.
- CHI3L2 represents a potential therapeutic target for glioblastoma treatment.
