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Updated: Dec 19, 2025

An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
MIR22HG regulates miR-486/PTEN axis in bladder cancer to promote cell proliferation
Qisheng Tang1, Xue Jiang2, Shanjin Ma1
1Department of Urology, Tangdu Hospital, Air Force Medical University, Xi'an City, Shaanxi Province 710038, China.
Abstract:
The tumor suppressive role of MIR22HG has been studied in several types of cancer. We analyzed the TCGA dataset and found the down-regulation of MIR22HG in bladder cancer (BC). Bioinformatics analysis predicted the interaction between MIR22HG and miR-486. The direct interaction between MIR22HG and miR-486 was also confirmed by dual luciferase assay. However, overexpression of these two factors did not significantly affect the expression of each other. Interestingly, overexpression of MIR22HG led to up-regulated phosphatase and tensin homolog (PTEN), which is a target of miR-486. In cell proliferation assay, overexpression of MIR22HG and PTEN led to decreased rates of BC cell proliferation. Moreover, overexpression of miR-486 played an opposite role and attenuated the effects of overexpression of MIR22HG and PTEN. Therefore, MIR22HG regulates miR-486/PTEN axis to promote cell proliferation in BC.
Insights
MIR22HG suppresses bladder cancer (BC) by regulating the miR-486/PTEN axis. Down-regulation of MIR22HG promotes BC cell proliferation, while its overexpression inhibits it.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The tumor-suppressive function of MIR22HG is recognized across various cancers.
- MIR22HG's role in bladder cancer (BC) pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of MIR22HG in bladder cancer.
- To explore the molecular mechanism of MIR22HG in regulating BC cell proliferation.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) dataset for MIR22HG expression in BC.
- Bioinformatics analysis and dual-luciferase reporter assays to confirm MIR22HG-miR-486 interaction.
- Cell proliferation assays to assess the functional impact of MIR22HG, PTEN, and miR-486.
Main Results:
- MIR22HG was found to be down-regulated in bladder cancer.
- MIR22HG directly interacts with miR-486 but does not affect its expression.
- MIR22HG overexpression up-regulates PTEN, inhibiting BC cell proliferation, an effect reversed by miR-486.
Conclusions:
- MIR22HG acts as a tumor suppressor in bladder cancer.
- MIR22HG regulates BC cell proliferation through the miR-486/PTEN axis.
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