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Updated: May 8, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MicroRNA-16 inhibits bladder cancer proliferation by targeting Cyclin D1
Qi-Quan Jiang1, Bin Liu, Tao Yuan
1Department of Urology, Affiliated Tongji Hospital, Tongji University, Shanghai, China.
Abstract:
MicroRNA-16 (miR-16) has been demonstrated to regulate proliferation and apoptosis in many types of cancers, but its biological function in bladder cancer remains unknown. Here, we found expression of miR-16 to be downregulated in bladder cancer in comparison with the adjacent normal tissues. Enforced expression of miR- 16 was able to inhibit cell proliferation in TCHu-1 cells, in line with results for miR-16 antisense oligonucleotides (antisense miR-16). At the molecular level, our results further revealed that cyclin D1 expression was negatively regulated by miR-16. Therefore, the data reported here demonstrate that miR-16 is an important regulator in bladder cancer, which will contribute to better understanding of important mis-regulated miRNAs.
Insights
MicroRNA-16 (miR-16) is downregulated in bladder cancer and inhibits cell proliferation by negatively regulating cyclin D1. This finding highlights miR-16 as a key regulator in bladder cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA-16 (miR-16) is implicated in cancer cell proliferation and apoptosis.
- The specific role of miR-16 in bladder cancer pathogenesis is not well understood.
Purpose of the Study:
- To investigate the expression and function of miR-16 in bladder cancer.
- To elucidate the molecular mechanisms underlying miR-16's role in bladder cancer.
Main Methods:
- Quantitative analysis of miR-16 expression in bladder cancer tissues versus normal tissues.
- Cell proliferation assays in bladder cancer cell lines (TCHu-1) with enforced miR-16 expression or antisense miR-16 treatment.
- Western blot analysis to assess the effect of miR-16 on cyclin D1 expression.
Main Results:
- miR-16 expression was significantly downregulated in bladder cancer tissues compared to adjacent normal tissues.
- Enforced expression of miR-16 inhibited bladder cancer cell proliferation, while antisense miR-16 promoted it.
- miR-16 directly targets and negatively regulates cyclin D1 expression at the molecular level.
Conclusions:
- miR-16 functions as a tumor suppressor in bladder cancer.
- The downregulation of miR-16 contributes to increased cell proliferation in bladder cancer, partly through the upregulation of cyclin D1.
- These findings identify miR-16 as a potential therapeutic target and biomarker for bladder cancer.
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Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
