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Updated: Sep 19, 2025

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
The lncRNA MIR22HG suppresses prostate cancer cell proliferation, migration, and epithelial-mesenchymal transition
Ansu Li1,2, Wu Sun3, Shihe Shao4
1Department of Clinical Laboratory, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Background:
Long non-coding RNAs (lncRNAs) play crucial roles in modulating the development and progression of human malignant cancers. As a tumour suppressor gene, the lncRNA MIR22HG has been identified in many kinds of cancers. However, the specific function of MIR22HG in prostate cancer (Pca) has yet to be elucidated. Specifically, we sought to determine whether MIR22HG plays a role in Pca progression and the underlying mechanisms involved.
Methods:
Differentially expressed lncRNAs in Pca tissues were screened by sequencing, and the expression of MIR22HG in cells and tissues was determined via quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK8), Transwell, and western blotting assays were used to determine whether Pca cell proliferation and migration can be regulated by the MIR22HG/microRNA-4428 (miR-4428)/PCDH9 axis. To investigate tumour growth in vivo, we constructed tumour subcutaneous xenograft models. Moreover, we performed bioinformatic analysis and dual-luciferase reporter assays to verify the expression of the miR-4428 and PCDH9 targets.
Results:
MIR22HG was expressed at low levels in Pca cells and tissues, and its upregulation inhibited cell proliferation and migration and prevented epithelial-mesenchymal transition (EMT) in vivo and in vitro. A negative correlation was found between MIR22HG expression and miR-4428 expression. The downstream target gene of miR-4428 was PCDH9. Therefore, MIR22HG may function as a competing endogenous RNA (ceRNA) to regulate miR-4428/PCDH9.
Conclusions:
We demonstrated that MIR22HG acts as a tumour suppressor in Pca and suggested that targeting the MIR22HG/miR-4428/PCDH9 axis may be a new avenue for Pca therapy.
Insights
Long non-coding RNA MIR22HG acts as a tumor suppressor in prostate cancer (Pca). Upregulating MIR22HG inhibits Pca progression by regulating the miR-4428/PCDH9 pathway, offering a potential new therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are critical in cancer development.
- MIR22HG, a lncRNA tumor suppressor, has an unelucidated role in prostate cancer (Pca).
- This study investigates MIR22HG's function and mechanisms in Pca progression.
Purpose of the Study:
- To determine the role of MIR22HG in prostate cancer progression.
- To elucidate the underlying molecular mechanisms of MIR22HG in Pca.
- To explore MIR22HG as a potential therapeutic target for Pca.
Main Methods:
- lncRNA expression profiling in Pca tissues via sequencing.
- Quantitative real-time polymerase chain reaction (qRT-PCR) for MIR22HG expression analysis.
- Cell proliferation, migration assays (CCK8, Transwell), western blotting, xenograft models, bioinformatic analysis, and dual-luciferase reporter assays to investigate the MIR22HG/miR-4428/PCDH9 axis.
Main Results:
- MIR22HG is downregulated in Pca tissues and cells.
- MIR22HG upregulation suppresses Pca cell proliferation, migration, and epithelial-mesenchymal transition (EMT) in vitro and in vivo.
- MIR22HG functions as a competing endogenous RNA (ceRNA) by sponging miR-4428, thereby regulating its target gene PCDH9.
Conclusions:
- MIR22HG functions as a tumor suppressor in prostate cancer.
- The MIR22HG/miR-4428/PCDH9 axis represents a novel therapeutic target for Pca treatment.
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