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Updated: Oct 22, 2025
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Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
Published on: December 31, 2014
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MEX3D is an oncogenic driver in prostate cancer
Longjiang Shao1,2, Jianghua Wang1,2, Omer Karatas1,2
1Department of Pathology & Immunology, Baylor College of Medicine, Houston, Texas, USA.
The Prostate
|August 29, 2021
Summary
Prostate cancer involves genetic changes like PTEN loss and TMPRSS2/ERG (TE) fusion. These alterations upregulate MEX3D and TCF3, promoting cancer growth and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer (PCa) is a leading cause of cancer death in the US.
- Common PCa genetic alterations include TMPRSS2/ERG (TE) fusion and PTEN loss.
- Mechanisms of cooperative transformation by these alterations are not fully understood.
Purpose of the Study:
- Investigate the role of MEX3D in prostate cancer.
- Determine the relationship between MEX3D, PTEN, TE fusion, and TCF3.
- Characterize the biological impact of MEX3D and TCF3 in PCa.
Main Methods:
- Microarray expression analysis of immortalized prostate cells.
- In silico and patient sample analysis of MEX3D expression in PCa.
- In vitro and in vivo studies to assess MEX3D and TCF3 functions.
- TCGA PanCancer database analysis to identify MEX3D targets.
Main Results:
- MEX3D is highly upregulated in PCa, associated with PTEN loss and TE fusion.
- MEX3D drives soft agar colony formation, invasion, and tumor formation in vivo.
- TCF3 is a major target of MEX3D in PCa, promoting invasion and colony formation.
Conclusions:
- PTEN loss and TE fusion in PCa upregulate MEX3D and TCF3.
- This MEX3D-TCF3 pathway promotes cancer transformation phenotypes.
- MEX3D and TCF3 are key players in prostate cancer progression.
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