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Updated: Jan 5, 2026

An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Silencing TTK expression inhibits the proliferation and progression of prostate cancer
Saipeng Chen1, Jianan Wang1, Lin Wang1
1Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300211, China.
Purpose:
The main objective of our study was to explore changes in the expression levels of differentially expressed genes associated with prostate cancer progression and to design a series of experiments to verify the function of differentially expressed genes.
Method:
The transcriptome datas of 499 cases of prostate cancer patients was downloaded from TCGA database. Differential genes associated with Gleason score were selected and filtered out by p < 0.05 and spearman coefficient >0.3. KEGG signaling pathway was enriched by differentially expressed genes, and TTK was selected as the research object. The expression of TTK was tested in prostate cancer tissues and prostate cancer cell lines. The changes of biological behavior of prostate cancer cell lines were verified after TTK was knocked out by siRNA and tumorigenic effect of TTK was verified by shRNA in vivo experiments.
Result:
The expression of TTK was positively correlated with Gleason score of prostate cancer, and the expression of protein and mRNA in metastatic prostate cancer cell lines was higher than that in non-metastatic prostate cancer cell lines. Vitro biological experiments showed that TTK gene knockout could inhibit the proliferation, invasion and migration of PC3 and DU145 cells, and promote cell apoptosis. In vivo experiments showed that TTK knockout inhibited tumorigenesis in mice. It was found that the expression of CDK2 and CCNE1 decreased after TTK was knocked out.
Conclusion:
Our results suggest that TTK is a gene associated with malignancy of PCa and could be a novel therapeutic target for clinical application.
Insights
The study found that TTK gene expression correlates with prostate cancer malignancy. Inhibiting TTK in cells and animal models reduced tumor growth, suggesting TTK as a potential therapeutic target for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate cancer (PCa) progression is linked to changes in gene expression.
- Identifying key genes driving PCa malignancy is crucial for developing new therapies.
Purpose of the Study:
- To investigate differentially expressed genes in prostate cancer progression.
- To functionally validate the role of selected genes, specifically TTK, in PCa.
Main Methods:
- Transcriptome analysis of 499 PCa cases from TCGA database.
- Selection and functional validation of TTK using siRNA and shRNA in PCa cell lines and in vivo models.
- KEGG pathway enrichment analysis.
Main Results:
- TTK expression positively correlates with Gleason score and is higher in metastatic PCa cell lines.
- TTK knockout inhibited PCa cell proliferation, invasion, migration, and promoted apoptosis in vitro.
- TTK knockout suppressed tumor formation in vivo and affected CDK2 and CCNE1 expression.
Conclusions:
- TTK is significantly associated with prostate cancer malignancy.
- TTK represents a potential novel therapeutic target for prostate cancer treatment.
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