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MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent
Published on: September 3, 2013
Inhibition of miR-9-5p suppresses prostate cancer progress by targeting StarD13
Lin Chen1, Weifeng Hu1, Guohao Li1
1Department of Urology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, No. 26 Shengli Street, Jiang'an District, Wuhan, 430014 China.
Background:
This study aims to investigate the effects of inhibiting microRNA-9-5p (miR-9-5p) on the expression of StAR-related lipid transfer domain containing 13 (StarD13) and the progress of prostate cancer.
Methods:
The mRNA expression levels of miR-9-5p and StarD13 were determined in several prostate cancer cell lines. We chose DU145 and PC-3 cells for further research. The CCK8 assay was used to measure the cell viability. The cell invasion and wound-healing assays were respectively applied to evaluate invasion and migration. The expression of E-cadherin (E-cad), N-cadherin (N-cad) and vimentin were measured via western blot. DU145 and PC-3 cells overexpressing StarD13 were generated to investigate the variation in proliferation, invasion and migration. A luciferase reporter assay was used to identify the target of miR-9-5p.
Results:
Our results show that miR-9-5p was highly expressed and StarD13 was suppressed in prostate cancer cells. MiR-9-5p inhibition repressed the cells' viability, invasion and migration. It also increased the expression of E-cad and decreased that of N-cad and vimentin. StarD13 overexpression gave the same results as silencing of miR-9-5p: suppression of cell proliferation, invasion and migration. The bioinformatics analysis predicted StarD13 as a target gene of miR-9-5p. Quantitative RT-PCR, western blot analysis and the dual-luciferase reporter assay were employed to confirm the prediction.
Conclusion:
Our results show that miR-9-5p plays a powerful role in the growth, invasion, migration and epithelial-mesenchymal transition (EMT) of prostate cancer cells by regulating StarD13. A therapeutic agent inhibiting miR-9-5p could act as a tumor suppressor for prostate cancer.
Insights
Inhibiting microRNA-9-5p (miR-9-5p) suppresses prostate cancer progression by increasing StarD13 expression. This finding suggests miR-9-5p inhibition as a potential therapeutic strategy for prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Prostate cancer is a significant health concern.
- The role of microRNAs in cancer progression is increasingly recognized.
- MicroRNA-9-5p (miR-9-5p) and Star-related lipid transfer domain containing 13 (StarD13) are implicated in cancer, but their specific interaction in prostate cancer requires elucidation.
Purpose of the Study:
- To investigate the effect of inhibiting miR-9-5p on StarD13 expression in prostate cancer.
- To determine the impact of miR-9-5p inhibition on prostate cancer cell behavior, including proliferation, invasion, and migration.
- To identify StarD13 as a direct target of miR-9-5p.
Main Methods:
- Quantitative RT-PCR and Western blot were used to measure miR-9-5p and StarD13 mRNA and protein levels in prostate cancer cell lines (DU145, PC-3).
- Cell viability, invasion, and migration were assessed using CCK8, invasion, and wound-healing assays, respectively.
- Luciferase reporter assays and overexpression studies were conducted to confirm the regulatory relationship between miR-9-5p and StarD13.
Main Results:
- miR-9-5p was found to be highly expressed while StarD13 was suppressed in prostate cancer cells.
- Inhibition of miR-9-5p significantly reduced prostate cancer cell viability, invasion, and migration.
- Overexpression of StarD13 mimicked the effects of miR-9-5p inhibition, suppressing cancer cell proliferation and metastasis, confirming StarD13 as a direct target of miR-9-5p.
Conclusions:
- miR-9-5p promotes prostate cancer growth, invasion, migration, and epithelial-mesenchymal transition (EMT) by downregulating StarD13.
- Targeting miR-9-5p represents a promising therapeutic strategy for prostate cancer, acting as a tumor suppressor.
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