Related Experiment Video
Updated: Feb 5, 2026

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
Published on: March 14, 2014
The putative tumour suppressor miR-1-3p modulates prostate cancer cell aggressiveness by repressing E2F5 and PFTK1
Sen-Mao Li1,2, Huan-Lei Wu3, Xiao Yu1
1Department of Urology, Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Liberalization Ave, No. 1095, Wuhan, 430030, People's Republic of China.
Background:
Previous studies report that miR-1-3p, a member of the microRNA-1 family (miR-1), and functions as a tumor suppressor in several different cancers. However, little is known regarding the biological role and intrinsic regulatory mechanisms of miR-1-3p in prostate cancer (PCa).
Methods:
In this study, the expression levels of miR-1-3p were first examined in PCa cell lines and tumor tissues by RT-qPCR and bioinformatics. The in vitro and in vivo functional effect of miR-1-3p was examined further. A luciferase reporter assay was conducted to confirm target associations.
Results:
We found that miR-1-3p was significantly downregulated in advanced PCa tissues and cell lines. Low miR-1-3p levels were strongly associated with aggressive clinicopathological features and poor prognosis in PCa patients. Ectopic expression of miR-1-3p in 22RV1 and LncaP cells was sufficient to prevent tumor cell growth and cell cycle progression in vitro and in vivo. Further mechanistic studies revealed that miR-1-3p could directly target the mRNA 3'- untranslated region (3'- UTR) of two central cell cycle genes, E2F5 and PFTK1, and could suppress their mRNA and protein expression. In addition, knockdown of E2F5 and PFTK1 mimicked the tumor-suppressive effects of miR-1-3p overexpression on PCa progression. Conversely, concomitant knockdown of miR-1-3p and E2F5 and PFTK1 substantially reversed the inhibitory effects of either E2F5 or PFTK1 silencing alone.
Conclusion:
These data highlight an important role for miR-1-3p in the regulation of proliferation and cell cycle in the molecular etiology of PCa and indicate the potential for miR-1-3p in applications furthering PCa prognostics and therapeutics.
Insights
MicroRNA-1-3p (miR-1-3p) acts as a tumor suppressor in prostate cancer (PCa) by downregulating E2F5 and PFTK1, inhibiting cell growth and progression. This finding suggests miR-1-3p as a potential biomarker and therapeutic target for PCa.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression.
- miR-1-3p, a member of the miRNA-1 family, is recognized as a tumor suppressor in various cancers.
- The specific role and regulatory mechanisms of miR-1-3p in prostate cancer (PCa) remain largely unexplored.
Purpose of the Study:
- To investigate the expression levels and biological functions of miR-1-3p in prostate cancer.
- To elucidate the molecular mechanisms underlying miR-1-3p's role in PCa progression.
- To assess the potential of miR-1-3p as a prognostic biomarker and therapeutic target for PCa.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) and bioinformatics analyses were employed to determine miR-1-3p expression in PCa cell lines and tissues.
- In vitro and in vivo functional assays were conducted to evaluate the effects of miR-1-3p on tumor cell growth and cell cycle progression.
- Luciferase reporter assays were utilized to confirm the direct targeting of E2F5 and PFTK1 by miR-1-3p.
Main Results:
- miR-1-3p was found to be significantly downregulated in advanced PCa tissues and cell lines, correlating with aggressive clinicopathological features and poor patient prognosis.
- Overexpression of miR-1-3p suppressed tumor cell proliferation and cell cycle progression both in vitro and in vivo.
- miR-1-3p directly targets the 3'-untranslated region (3'-UTR) of E2F5 and PFTK1, leading to decreased expression of these cell cycle regulatory genes.
Conclusions:
- miR-1-3p plays a crucial role in regulating cell proliferation and cell cycle progression in prostate cancer.
- The downregulation of miR-1-3p contributes to the molecular etiology of PCa.
- miR-1-3p holds promise as a potential biomarker for PCa prognosis and a therapeutic target for PCa treatment.
Related Concept Videos
Aggression
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Repressed Memory
Repressible Operon: trp Operon
Loss of Tumor Suppressor Gene Functions
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Secondary Motives: Affiliation Motivation and Aggression Motivation

