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Updated: Feb 5, 2026

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
Published on: January 9, 2019
EYA4 Promotes Cell Proliferation Through Downregulation of p27Kip1 in Glioma
Zhaoming Li1, Ran Qiu2, Xia Qiu3
1Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Background/Aims:
Accumulating evidence suggests that Eyes Absent Homologue 4 (EYA4) plays an important role in tumorigenesis and progression of various cancers. However, the role of EYA4 in glioma development is still unclear.
Methods:
The expression of EYA4 was examined in glioma tissues by immunohistochemistry. Cell viability and apoptosis were analyzed by CCK-8, BrdU assay, and flow cytometry.
Results:
We found that EYA4 was upregulated in glioma, and its expression was positively correlated with advanced tumor stage. Moreover, higher expression of EYA4 predicted a worse overall survival in patients with glioma. Forced overexpression of EYA4 enhanced glioma cell proliferation, and EYA4 suppressed the expression of p27Kip1 directly in these cells. Furthermore, Six1 was required for EYA4 to suppress the expression of p27Kip1 in glioma.
Conclusion:
Together, we demonstrate that EYA4 promotes cell proliferation by directly suppressing the expression of p27Kip1 in glioma.
Insights
Eyes Absent Homologue 4 (EYA4) promotes glioma cell proliferation by suppressing p27Kip1 expression. Upregulated EYA4 correlates with advanced glioma stages and predicts poorer patient survival, highlighting its oncogenic role.
Area of Science:
- Neuro-oncology
- Molecular oncology
- Cancer biology
Background:
- Eyes Absent Homologue 4 (EYA4) is implicated in various cancers.
- The specific role of EYA4 in glioma pathogenesis remains largely undefined.
Purpose of the Study:
- To investigate the expression and function of EYA4 in glioma.
- To elucidate the molecular mechanisms underlying EYA4's role in glioma development.
Main Methods:
- Immunohistochemistry to assess EYA4 expression in glioma tissues.
- Cell viability assays (CCK-8, BrdU) and flow cytometry to analyze cell proliferation and apoptosis.
- Western blotting to examine protein expression levels, including p27Kip1 and Six1.
Main Results:
- EYA4 expression is upregulated in glioma tissues and positively correlates with advanced tumor stage.
- Higher EYA4 expression is associated with worse overall survival in glioma patients.
- Overexpression of EYA4 enhances glioma cell proliferation by directly suppressing p27Kip1 expression, a process dependent on Six1.
Conclusions:
- EYA4 acts as an oncoprotein in glioma, promoting cell proliferation.
- The mechanism involves the direct suppression of p27Kip1 expression, mediated by Six1.
- EYA4 represents a potential therapeutic target for glioma.
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