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Updated: Mar 18, 2026

Magnetic Resonance Imaging Assessment of Carcinogen-induced Murine Bladder Tumors
Published on: March 29, 2019
MicroRNA‑335 inhibits bladder cancer cell growth and migration by targeting mitogen‑activated protein kinase 1
Xiaolin Wang1, Guang Wu2, Guangxin Cao1
1Department of Urology, Nantong Tumor Hospital, Nantong, Jiangsu 226361, P.R. China.
Abstract:
The abnormal expression of microRNAs (miRs) as oncogenes or tumor‑suppressor genes has been widely investigated in various tumor types. However, the roles of miR‑335 in bladder cancer cells have remained elusive. The aim of the present study was to assess the expression of miR‑335 in bladder cancer as well as the effects of miR‑335 on bladder cancer cell proliferation, metastasis and apoptosis. PCR and western blot analyses revealed that miR‑335 was significantly downregulated in bladder cancer tissues, and low levels of miR‑335 were associated with more aggressive phenotypes of bladder cancer. Overexpression of miR‑335 in T24 cells inhibited cell proliferation and induced apoptosis as indicated by an MTT assay and flow cytometric analysis, respectively. Furthermore, overexpression of miR‑335 significantly suppressed cell migration, as indicated by a Transwell assay. The expression of mitogen‑activated protein kinase (MAPK)1 was decreased after overexpression of miR‑335, indicating that MAPK1 may be a target gene of miR‑335. In addition, silencing of MAPK1 inhibited the proliferation and migration of bladder cancer cells. In conclusion, the results of the present study demonstrated that miR‑335 was significantly downregulated in bladder cancer, and may act as a tumor suppressor through repression of MAPK1.
Insights
MicroRNA-335 (miR-335) is downregulated in bladder cancer, acting as a tumor suppressor. Its reduced expression correlates with aggressive cancer, while restoring miR-335 inhibits proliferation and metastasis by targeting MAPK1.
Area of Science:
- Molecular Oncology
- Cancer Biology
Background:
- MicroRNAs (miRs) play critical roles as oncogenes or tumor suppressors in various cancers.
- The specific function of miR-335 in bladder cancer remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression levels of miR-335 in bladder cancer tissues.
- To determine the impact of miR-335 on bladder cancer cell proliferation, apoptosis, and metastasis.
- To identify potential molecular targets of miR-335 in bladder cancer.
Main Methods:
- Quantitative PCR and Western blot analysis to assess miR-335 and MAPK1 expression.
- MTT assay for cell proliferation assessment.
- Flow cytometry for apoptosis analysis.
- Transwell assay for cell migration evaluation.
- Gene silencing techniques to validate target interactions.
Main Results:
- miR-335 was significantly downregulated in bladder cancer tissues, with lower levels associated with aggressive disease phenotypes.
- Overexpression of miR-335 inhibited T24 bladder cancer cell proliferation and induced apoptosis.
- Restoring miR-335 levels suppressed cell migration and invasion.
- Mitogen-activated protein kinase (MAPK)1 expression was reduced upon miR-335 overexpression, suggesting MAPK1 as a direct target.
- Silencing MAPK1 mimicked the inhibitory effects of miR-335 on proliferation and migration.
Conclusions:
- miR-335 functions as a tumor suppressor in bladder cancer.
- The tumor-suppressive role of miR-335 is mediated, at least in part, through the repression of MAPK1.
- miR-335 represents a potential therapeutic target for bladder cancer treatment.
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