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Updated: Mar 3, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
SOX4 induces tumor invasion by targeting EMT-related pathway in prostate cancer
Yifan Liu1, Shan Zeng2, Xianhan Jiang1
11 Department of Urology, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Abstract:
SOX4 (sex-determining region Y-related high-mobility group box 4) is associated with tumor progression and poor clinical outcome in several cancers. This study aims to evaluate whether SOX4 affects the biological behaviors of prostate cancer and further elucidate whether this effect works through the epithelial-mesenchymal transition pathway. We investigated the expression of SOX4 in a series of prostate cancer tissues and adjacent noncancerous tissues, as well as in a panel of prostate cancer cell lines. Cell proliferation, migration, and invasion were evaluated in SOX4 knockdown prostate cancer cell lines by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assay. Our results showed that the expression of SOX4 was remarkably upregulated both in prostate cancer tissues and in cell lines. Knockdown of SOX4 repressed the ability of cell proliferation and migration of DU145 cells. Moreover, inhibition of SOX4 could reverse the epithelial-mesenchymal transition processes through upregulation of E-cadherin and downregulation of vimentin. This study provided evidence that SOX4 could serve as a potential therapeutic target in prostate cancer.
Insights
Sex-determining region Y-related high-mobility group box 4 (SOX4) drives prostate cancer progression. Inhibiting SOX4 reduces cancer cell proliferation and migration, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Sex-determining region Y-related high-mobility group box 4 (SOX4) is implicated in tumor progression and poor outcomes across various cancers.
- The role of SOX4 in prostate cancer's biological behaviors and its potential link to the epithelial-mesenchymal transition (EMT) pathway require further investigation.
Purpose of the Study:
- To determine the expression levels of SOX4 in prostate cancer tissues and cell lines.
- To evaluate the impact of SOX4 on prostate cancer cell proliferation, migration, and invasion.
- To elucidate the mechanism by which SOX4 influences prostate cancer, specifically through the epithelial-mesenchymal transition (EMT) pathway.
Main Methods:
- SOX4 expression was analyzed in prostate cancer tissues and adjacent noncancerous tissues, alongside a panel of prostate cancer cell lines.
- Prostate cancer cell lines with SOX4 knockdown were subjected to proliferation, migration, and invasion assays (e.g., MTT and Transwell assays).
- Changes in epithelial-mesenchymal transition (EMT) markers, E-cadherin and vimentin, were assessed following SOX4 inhibition.
Main Results:
- SOX4 expression was significantly upregulated in both prostate cancer tissues and cell lines compared to normal controls.
- Knockdown of SOX4 expression markedly repressed the proliferation and migration capabilities of DU145 prostate cancer cells.
- Inhibition of SOX4 reversed EMT processes, evidenced by increased E-cadherin and decreased vimentin expression.
Conclusions:
- SOX4 is overexpressed in prostate cancer and promotes key cancer cell behaviors like proliferation and migration.
- SOX4 appears to mediate its effects, at least in part, through the regulation of the epithelial-mesenchymal transition pathway.
- SOX4 represents a promising therapeutic target for the treatment of prostate cancer.
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