Oncotarget

Research Papers:

Knockdown of long non-coding RNA Taurine Up-Regulated 1 inhibited doxorubicin resistance of bladder urothelial carcinoma via Wnt/β-catenin pathway

Dalong Xie, Hui Zhang, Xuanhao Hu and Chao Shang _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:88689-88696. https://doi.org/10.18632/oncotarget.20927

Metrics: PDF 1372 views  |   HTML 1748 views  |   ?  


Abstract

Dalong Xie1, Hui Zhang2, Xuanhao Hu3 and Chao Shang3

1Department of Anatomy, College of Basic Medicine, China Medical University, Shenyang, 110001, China

2Department of Urinary surgery, Shengjing Hospital, China Medical University, Shenyang, 110004, China

3Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang, 110001, China

Correspondence to:

Chao Shang, email: [email protected]

Keywords: bladder urothelial carcinoma, long noncoding RNA, Taurine Up-Regulated 1, chemotherapy, Wnt/β-catenin pathway

Received: July 20, 2017     Accepted: August 29, 2017     Published: September 15, 2017

ABSTRACT

In genitourinary system, bladder cancer (BC) is the most common and lethal malignant tumor, which most common type is bladder urothelial carcinoma (BUC). Long non-coding RNA (lncRNA) Taurine Up-Regulated 1 (TUG1) gene is high-expressed in several malignant tumors, including BC. In this study, over-expression of TUG1 was found in BUC tissues and cell line resistant to doxorubicin (Dox). Knockdown of TUG1 inhibited the Dox resistance and promoted the cytotoxicity induced by Dox in T24/Dox cells. TUG1 knockdown also depressed the Wnt/β-catenin pathway, and the activation the Wnt/β-catenin pathway partly reversed the inhibitory effects of TUG1 knockdown on Dox resistance in T24/Dox cells. In conclusion, up-regulation of lncRNA TUG1 was related with the poor response of BUC patients to Dox chemotherapy, knockdown of TUG1 inhibited the Dox resistance of BUC cells via Wnt/β-catenin pathway. These findings might assist in the discovery of novel potential diagnostic and therapeutic target for BUC, thereby improve the effects of clinical treatment in patients.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 20927