Related Experiment Video
Updated: Jul 13, 2026
Mouse Bladder Wall Injection
Published on: July 12, 2011
MiR-122 targets VEGFC in bladder cancer to inhibit tumor growth and angiogenesis
Yi Wang1, Qing-Fei Xing1, Xiao-Qiang Liu1
1Department of Urology, The Second Hospital of Tianjin Medical University, Tianjin Institute of Urology No. 23, Pingjiang Road, Hexi District, Tianjin 300211, China.
Abstract:
Previous studies indicate that microRNA-122 (miR-122) is down-regulated in several cancer cells and regulates cell apoptosis, proliferation, metastasis, and tumor angiogenesis. However, the mount of miR-122 in bladder cancer and the pivotal molecular mechanisms of miR-122 used to regulate bladder carcinogenesis and angiogenesis remain to be clarified. Here, we reveal that miR-122 expression is down-regulated in human bladder cancer tissues and cell lines. MiR-122 represses vascular endothelial growth factor C (VEGFC) post-transcriptional expression by directly binding to its 3'-UTR. The protein kinase B (AKT) and mammalian target of rapamycin (mTOR), which are the most important downstream molecules of VEGFC, are also decreased in bladder cancer cell after miR-122 overexpression. Furthermore, miR-122 over-expression decreases bladder cancer cell migration, invasion, colony formation in vitro and slow bladder cancer growth and angiogenesis in vivo. Finally, miR-122 sensitizes bladder cancer cells to cisplatin-induced apoptosis. Taken together, these studies suggest that miR-122 serves as a tumor suppressor and down-regulating VEGFC expression, leading to the inhibition of bladder cancer growth and angiogenesis.
Insights
MicroRNA-122 (miR-122) is reduced in bladder cancer, suppressing tumor growth and angiogenesis by targeting VEGFC. Overexpressing miR-122 inhibits cancer cell migration and sensitizes cells to cisplatin.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNA-122 (miR-122) is implicated in various cancers, regulating apoptosis, proliferation, metastasis, and angiogenesis.
- The specific role and mechanisms of miR-122 in bladder cancer progression and angiogenesis require further elucidation.
Purpose of the Study:
- To investigate the expression levels of miR-122 in bladder cancer.
- To clarify the molecular mechanisms by which miR-122 regulates bladder carcinogenesis and angiogenesis.
Main Methods:
- Quantitative analysis of miR-122 expression in human bladder cancer tissues and cell lines.
- Luciferase reporter assays to confirm direct binding of miR-122 to the 3'-UTR of VEGFC.
- In vitro assays (migration, invasion, colony formation) and in vivo studies to assess the impact of miR-122 overexpression on tumor growth and angiogenesis.
- Assessment of downstream signaling pathways (AKT, mTOR) and chemosensitivity to cisplatin.
Main Results:
- miR-122 expression is significantly down-regulated in human bladder cancer.
- miR-122 directly represses vascular endothelial growth factor C (VEGFC) expression.
- Overexpression of miR-122 reduces VEGFC, AKT, and mTOR signaling, inhibiting bladder cancer cell migration, invasion, colony formation, growth, and angiogenesis.
- miR-122 enhances cisplatin-induced apoptosis in bladder cancer cells.
Conclusions:
- miR-122 functions as a tumor suppressor in bladder cancer.
- Down-regulation of miR-122 contributes to bladder cancer progression and angiogenesis via VEGFC.
- miR-122 represents a potential therapeutic target for bladder cancer treatment.
