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Updated: Oct 22, 2025
Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
Published on: December 31, 2014
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.
Background:
Prostate cancer (PCa) is the most common visceral malignancy and the second leading cause of cancer deaths in US men. The two most common genetic alterations in PCa are expression of the TMPRSS2/ERG (TE) fusion gene and loss of the PTEN tumor suppressor. These genetic alterations act cooperatively to transform prostatic epithelium but the exact mechanisms involved are unclear.
Methods:
Microarray expression analysis of immortalized prostate epithelial cells transformed by loss of PTEN and expression of the TE fusion revealed MEX3D as one of the most highly upregulated genes. MEX3D expression in prostate cancer was examined in patient samples and in silico. In vitro and in vivo studies to characterize the biological impact of MEX3D were carried out. Analysis of the TCGA PanCancer database revealed TCF3 as a major target of MEX3D. The induction of TCF3 by MEX3D was confirmed and the biological impact of TCF3 examined by in vitro studies.
Results:
MEX3D is expressed at increased levels in prostate cancer and is increased by decreased PTEN and/or expression of the TE fusion gene and drives soft agar colony formation, invasion and tumor formation in vivo. The known oncogenic transcription factor TCF3 is highly correlated with MEX3D in prostate cancer. MEX3D expression strongly induces TCF3, which promotes soft agar colony formation and invasion in vitro.
Conclusions:
Loss of PTEN and expression of the TE fusion gene in prostate cancer strongly upregulates expression of MEX3D and its target TCF3 and promotes transformation associated phenotypes via this pathway.
Insights
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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