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Down-regulation of LncRNA TUG1 enhances radiosensitivity in bladder cancer via suppressing HMGB1 expression
Huijuan Jiang1, Xigang Hu2, Hongzhi Zhang2
1Department of Radiotherapy, Huaihe Hospital of Henan University, No.1 Baobei Road, Gulou District, Kaifeng, 475000, China. juanjiangh@163.com.
Background:
Long non-coding RNAs (lncRNAs) have been reported to regulate the sensitivity of different cancer cells to chemoradiotherapy. Aberrant expression of lncRNA Taurine-upregulated gene 1 (TUG1) has been found to be involved in the development of bladder cancer, however, its function and underlying mechanism in the radioresistance of bladder cancer remains unclear.
Methods:
Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of TUG1 and HMGB1 mRNA in bladder cancer tissues and cell lines. HMGB1 protein levels were tested by western blot assays. Different doses of X-ray were used for radiation treatment of bladder cancer cells. Colony survival and cell viability were detected by clonogenic assay and CCK-8 Kit, respectively. Cell apoptosis was determined by flow cytometry. A xenograft mouse model was constructed to observe the effect of TUG1 on tumor growth in vivo.
Results:
The levels of TUG1 and HMGB1 were remarkably increased in bladder cancer tissues and cell lines. Radiation treatment markedly elevated the expression of TUG1 and HMGB1. TUG1 knockdown inhibited cell proliferation, promoted cell apoptosis and decreased colony survival in SW780 and BIU87 cells under radiation. Moreover, TUG1 depletion suppressed the HMGB1 mRNA and protein levels. Furthermore, overexpression of HMGB1 reversed TUG1 knockdown-induced effect in bladder cancer cells. Radiation treatment dramatically reduced the tumor volume and weight in xenograft model, and this effect was more obvious when combined with TUG1 silencing.
Conclusion:
LncRNA TUG1 knockdown enhances radiosensitivity of bladder cancer by suppressing HMGB1 expression. TUG1 acts as a potential regulator of radioresistance of bladder cancer, and it may represent a promising therapeutic target for bladder cancer patients.
Insights
Knocking down long non-coding RNA Taurine-upregulated gene 1 (TUG1) enhances bladder cancer radiosensitivity by suppressing HMGB1. TUG1 is a potential therapeutic target for improving bladder cancer treatment outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) influence cancer cell sensitivity to chemoradiotherapy.
- Aberrant expression of lncRNA Taurine-upupregulated gene 1 (TUG1) is implicated in bladder cancer development.
- The precise role and mechanism of TUG1 in bladder cancer radioresistance remain unclear.
Purpose of the Study:
- To investigate the function and mechanism of lncRNA TUG1 in the radioresistance of bladder cancer.
- To determine if TUG1 affects bladder cancer cell sensitivity to radiation therapy.
- To explore the potential of TUG1 as a therapeutic target for bladder cancer.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and western blot assays were used to measure TUG1 and HMGB1 expression.
- Bladder cancer cells were treated with X-ray radiation, and outcomes were assessed using clonogenic assays, CCK-8 kits, and flow cytometry.
- A xenograft mouse model was employed to evaluate the in vivo effects of TUG1 on tumor growth.
Main Results:
- TUG1 and HMGB1 expression were significantly elevated in bladder cancer tissues and cells, and further increased by radiation.
- TUG1 knockdown reduced cell proliferation, enhanced apoptosis, and decreased colony survival under radiation.
- TUG1 depletion suppressed HMGB1 levels, while HMGB1 overexpression counteracted the effects of TUG1 knockdown; TUG1 silencing amplified the anti-tumor effects of radiation in vivo.
Conclusions:
- LncRNA TUG1 knockdown enhances bladder cancer radiosensitivity by suppressing HMGB1 expression.
- TUG1 plays a regulatory role in bladder cancer radioresistance.
- TUG1 represents a promising therapeutic target for bladder cancer patients.
