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Updated: May 9, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR (qPCR)
Published on: May 16, 2012
A dosage-dependent pleiotropic role of Dicer in prostate cancer growth and metastasis
1Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA.
Abstract:
Dicer is an RNase III enzyme essential for the maturation of the majority of microRNAs. Recent studies have revealed downregulation or hemizygous loss of Dicer in many tumor models and demonstrated that suppressing Dicer activity enhances tumorigenic activities of lung and breast cancer cells, which support Dicer as a haploinsufficient tumor suppressor in these cancer models. Surprisingly, we found that knocking down Dicer expression suppresses the growth and tumorigenic capacity of human prostate cancer cell lines, but enhances migratory capacities of some prostate cancer cell lines. Dicer is upregulated in human prostate cancer specimens, but lower Dicer expression portends a shorter time to recurrence. Complete ablation of Dicer activity in a Pten null mouse model for prostate cancer significantly halts tumor growth and progression, demonstrating that microRNAs have a critical role in maintaining cancer cell fitness. In comparison, hemizygous loss of Dicer in the same model also reduces primary tumor burden, but induces a more locally invasive phenotype and causes seminal vesicle obstruction at high penetrance. Disrupting Dicer activity leads to an increase in apoptosis and senescence in these models, presumably through upregulation of P16/INK4a and P27/Kip1. Collectively, these results highlight a pleotropic role of Dicer in tumorigenesis that is not only dosage-dependent but also tissue context-dependent.
Insights
Dicer enzyme
Area of Science:
- Molecular Biology
- Cancer Research
- Biochemistry
Background:
- Dicer, an RNase III enzyme, is crucial for microRNA maturation.
- Dicer's role as a tumor suppressor is suggested by its downregulation in some cancers.
- Its function in prostate cancer remains incompletely understood.
Purpose of the Study:
- To investigate the role of Dicer in prostate cancer growth and metastasis.
- To determine the impact of Dicer activity levels on prostate cancer progression.
- To elucidate the mechanisms underlying Dicer's effects in prostate cancer.
Main Methods:
- Knockdown of Dicer expression in human prostate cancer cell lines.
- Analysis of Dicer's effect on cell growth, migration, and tumorigenicity.
- Utilizing a Pten null mouse model to study Dicer ablation and hemizygous loss in prostate cancer.
- Assessing apoptosis and senescence markers (P16/INK4a, P27/Kip1).
Main Results:
- Dicer knockdown suppressed growth but enhanced migration in some prostate cancer cells.
- Dicer is upregulated in human prostate cancer, with lower expression linked to shorter recurrence times.
- Complete Dicer ablation halted tumor growth in a Pten null model.
- Hemizygous Dicer loss reduced tumor burden but increased invasiveness and obstruction.
Conclusions:
- Dicer exhibits context- and dosage-dependent roles in prostate tumorigenesis.
- MicroRNAs processed by Dicer are critical for maintaining cancer cell fitness.
- Disrupting Dicer activity can induce apoptosis and senescence, impacting tumor progression.
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