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Updated: Dec 30, 2025

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
Published on: May 16, 2012
LINC00908 negatively regulates microRNA-483-5p to increase TSPYL5 expression and inhibit the development of prostate
1Department of Urology, China-Japan Union Hospital of Jilin University, No. 126, Xiantai Street, Changchun, 130033 Jilin People's Republic of China.
Background:
Accumulating evidence has associated aberrant long non-coding RNAs (lncRNAs) with various human cancers. This study aimed to explore the role of LINC00908 in prostate cancer (PCa) and its possible underlying mechanisms.
Methods:
Microarray data associated with PCa were obtained from the Gene Expression Omnibus (GEO) to screen the differentially expressed genes or lncRNAs. Then, the expression of LINC00908 in PCa tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The localization of LINC00908 in PCa cells was examined by fluorescence in situ hybridization (FISH). The relationship among LINC00908, microRNA (miR)-483-5p, and TSPYL5 was detected by bioinformatics analysis, dual-luciferase reporter assay, RNA pull-down, RNA binding protein immunoprecipitation (RIP), and FISH assays. Cell biological behaviors were assessed after the expression of LINC00908, miR-483-5p, and TSPYL5 was altered in PCa cells. Lastly, tumor growth in nude mice was evaluated.
Results:
Poorly expressed LINC00908 was witnessed in PCa tissues and cells. LINC00908 competitively bound to miR-483-5p to up-regulate the TSPYL5 expression. Overexpression of LINC00908 resulted in reduced PCa cell proliferation, migration and invasion, and promoted apoptosis. Additionally, the suppression on PCa cell proliferation, migration and invasion was induced by up-regulation of TSPYL5 or inhibition of miR-483-5p. In addition, in vivo experiments showed that overexpression of LINC00908 inhibited tumor growth of PCa.
Conclusion:
Overall, LINC00908 could competitively bind to miR-483-5p to increase the expression of TSPYL5, thereby inhibiting the progression of PCa. Therefore, LINC00908 may serve as a novel target for the treatment of PCa.
Insights
Long non-coding RNA LINC00908 acts as a tumor suppressor in prostate cancer (PCa) by regulating miR-483-5p and TSPYL5. Overexpression of LINC00908 inhibits PCa progression and tumor growth.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Aberrant expression of long non-coding RNAs (lncRNAs) is linked to human cancers.
- The specific role of LINC00908 in prostate cancer (PCa) requires further investigation.
Purpose of the Study:
- To investigate the role of LINC00908 in prostate cancer (PCa).
- To elucidate the underlying molecular mechanisms of LINC00908 in PCa progression.
Main Methods:
- Screening differentially expressed lncRNAs using Gene Expression Omnibus (GEO) microarray data.
- Assessing LINC00908 expression in PCa tissues and cell lines via RT-qPCR and FISH.
- Investigating the LINC00908/miR-483-5p/TSPYL5 interaction using bioinformatics, dual-luciferase reporter assays, RNA pull-down, RIP, and FISH.
- Evaluating the impact of altered gene expression on PCa cell behavior and tumor growth in vivo.
Main Results:
- LINC00908 expression was found to be downregulated in PCa tissues and cells.
- LINC00908 competitively binds to miR-483-5p, leading to increased TSPYL5 expression.
- Overexpression of LINC00908 suppressed PCa cell proliferation, migration, and invasion, while promoting apoptosis.
- TSPYL5 upregulation or miR-483-5p inhibition mimicked the tumor-suppressive effects of LINC00908.
- In vivo studies confirmed that LINC00908 overexpression inhibited PCa tumor growth.
Conclusions:
- LINC00908 functions as a tumor suppressor in PCa by modulating the miR-483-5p/TSPYL5 axis.
- LINC00908's ability to upregulate TSPYL5 expression inhibits PCa progression.
- LINC00908 presents a potential novel therapeutic target for prostate cancer treatment.
Related Concept Videos
MicroRNAs
MicroRNAs
Abnormal Proliferation
lncRNA - Long Non-coding RNAs

