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Updated: Mar 23, 2026
An Orthotopic Bladder Tumor Model and the Evaluation of Intravesical saRNA Treatment
Published on: July 28, 2012
shRNA targeting long non-coding RNA CCAT2 controlled by tetracycline-inducible system inhibits progression of bladder
Jianfa Li1,2, Chengle Zhuang1,2, Yuchen Liu1
1Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen, China.
Abstract:
Recent reports show that long non-coding RNAs (lncRNAs) are emerging as significant functional regulators in the development of tumors, including bladder cancer. Here, we found that CCAT2 was upregulated in bladder cancer tissues and cell lines. Through the statistical analyses, we also found that the high expression level of CCAT2 was positively correlated with histological grade and TNM stage of bladder cancer. Further experimental results revealed that knockdown of CCAT2 could decrease cell proliferation and migration as well as induce apoptosis in bladder cancer cells. Besides, using the post-transcriptional device of synthetic biology, we create the tetracycline-inducible double small hairpin RNAs (shRNAs) vector to control the expression level of CCAT2 which was induced by doxycycline in a dosage-dependent manner. In summary, our data indicated that CCAT2 may be an oncogene and a therapeutic target in bladder cancer. The expression of CCAT2 can be quantitatively controlled by the synthetic "tetracycline-on" switch system in bladder cancer in response to different concentrations of doxycycline to inhibit the development of bladder cancer cells.
Insights
CCAT2, a long non-coding RNA (lncRNA), is upregulated in bladder cancer, promoting tumor growth. Inhibiting CCAT2 with a novel synthetic biology system shows potential for bladder cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators in tumor development.
- Bladder cancer progression is influenced by dysregulated gene expression, including lncRNAs.
Purpose of the Study:
- To investigate the role of CCAT2 in bladder cancer.
- To explore CCAT2 as a potential therapeutic target for bladder cancer.
Main Methods:
- Quantitative analysis of CCAT2 expression in bladder cancer tissues and cell lines.
- Functional assays including cell proliferation, migration, and apoptosis after CCAT2 knockdown.
- Development of a doxycycline-inducible synthetic biology system to control CCAT2 expression.
Main Results:
- CCAT2 expression is significantly upregulated in bladder cancer tissues and cell lines.
- High CCAT2 expression correlates positively with advanced histological grade and TNM stage.
- CCAT2 knockdown suppresses bladder cancer cell proliferation and migration while inducing apoptosis.
- A synthetic "tetracycline-on" switch system effectively controlled CCAT2 expression in a doxycycline-dependent manner.
Conclusions:
- CCAT2 functions as an oncogene in bladder cancer.
- CCAT2 represents a potential therapeutic target for bladder cancer.
- The developed synthetic biology system offers a controllable method for modulating CCAT2 expression to inhibit bladder cancer progression.
