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Updated: May 9, 2026
Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
The miR-192/EGR1-HOXB9 loop inhibits immune evasion in glioma by arresting their NSC phenotypes
Guo-Wei Li1, Yan-Ping Jin2, Min-Feng Sheng3
1School of Rehabilitation Science, Nanjing Normal University of Special Education, Nanjing, Jiangsu 210038, China.
Objective:
To elucidate the mechanism by which the miR-192-related axis regulates glioma immune evasion.
Methods:
Factor expression was measured by PCR/Western Blotting (WB). Immunofluorescence, FISH and DLRTM were used to elucidate target regulation mechanisms. Mitophagy was observed by TEM. We performed BrdU/Transwell assays to evaluate malignant phenotypes and WB to measure stemness-related protein expression in glioma. Immune chemokine levels were measured by ELISA, and M2-TAM/CD8+ T-cell proportions were measured by immune-fluorescence. Growth curves/tumor volume in vivo and tumor weight in vitro were assessed to evaluate tumor growth in vivo. An immune microenvironment was established in nude mice via tail vein injection of immune cells. Masson's trichrome staining was performed to explore the degree of fibrosis in relevant tissues.
Results:
MiR-192 expression was negatively correlated with glioma malignancy. The expression of downstream regulator (EGR1/HOXB9) of miR-192 was positively correlated with malignant phenotypes. MiR-192 inhibited EGR1/HOXB9 through targeted binding. The miR-192/EGR1-HOXB9 loop induced mitophagy, thus inhibited glioma cell proliferation/invasion. Moreover, this loop inhibited MT, weakening glioma cell stemness. This pathway reduced M2-TAM numbers and weakened their inhibitory effect on CD8+ T-cells by regulating immune chemokines. In vivo, miR-192 inhibited glioma proliferation and induced immune infiltration into glioma through this loop.
Conclusion:
The miR-192/EGR1-HOXB9 loop inhibited glioma stemness phenotypes, weakening glioma malignancy by regulating mitophagy. Moreover, this loop affected chemokine secretion by TAMs, weakened their inhibitory effect on CD8+ T-cells and reduced immune evasion in glioma by regulating MT.
Insights
The miR-192/EGR1-HOXB9 loop suppresses glioma stemness and malignancy by inducing mitophagy. This pathway also enhances anti-tumor immunity by reducing myeloid-derived suppressor cells and increasing CD8+ T-cell activity.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Glioblastoma (glioma) is a highly aggressive brain tumor characterized by immune evasion.
- MicroRNAs (miRNAs) play critical roles in cancer development and progression, including in glioblastoma.
- Understanding the regulatory mechanisms of glioma immune evasion is crucial for developing effective therapies.
Purpose of the Study:
- To elucidate the molecular mechanism by which the miR-192-related axis regulates glioma immune evasion.
- To investigate the role of the miR-192/EGR1-HOXB9 pathway in controlling glioma malignancy and immune microenvironment.
Main Methods:
- Quantitative PCR and Western Blotting for factor expression analysis.
- Immunofluorescence, FISH, and DLRTM for target regulation studies.
- Transmission Electron Microscopy (TEM) for mitophagy observation.
- BrdU/Transwell assays for malignant phenotypes and stemness evaluation.
- ELISA and immune-fluorescence for immune chemokine and cell proportion analysis.
- In vivo and in vitro tumor growth assessments in nude mice models.
Main Results:
- MiR-192 expression was inversely correlated with glioma malignancy.
- The miR-192/EGR1-HOXB9 loop inhibited glioma cell proliferation, invasion, and stemness by inducing mitophagy and regulating mitochondrial function.
- This pathway modulated the tumor immune microenvironment by reducing M2-TAMs and enhancing CD8+ T-cell activity through chemokine regulation.
- In vivo studies confirmed that miR-192 inhibited tumor growth and promoted immune infiltration.
Conclusions:
- The miR-192/EGR1-HOXB9 loop is a key regulator of glioma malignancy and immune evasion.
- Targeting this loop could represent a novel therapeutic strategy to overcome glioma stemness and immune suppression.
- This pathway offers a potential target for enhancing anti-glioma immune responses.
