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Author Notes:

Corresponding Author: Xiangbo Kong, Kongxb@jlu.edu.cn Guangping Chen, gchen3@emory.edu

GC, RH, MA, BY, JS, and XK conception, design, data analysis, and interpretation; RH and MA – sample and data collection; RH, and GC –experimental execution; GC, RH, MA, and JS – manuscript writing; GC – final approval of manuscript.

We thank Otor Al-Khalili and Dr. Douglas Eaton for help with real-time PCR.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


Research Funding:

This work was supported by Emory URC grant (to GC) and NIH grants R01-DK087838 (to GC), and R01-DK89828 and R01-DK41707 (to JS)

Ruida Hou was supported by the China Scholarship Council (CSC) under the State Scholarship Fund.


  • Urothelium
  • Tumor
  • Urea transporter
  • Gene expression
  • Sialylation

Identification of a Novel UT-B Urea Transporter in Human Urothelial Cancer


Journal Title:

Frontiers in Physiology


Volume 8


, Pages 245-245

Type of Work:

Article | Final Publisher PDF


The urea transporter UT-B is widely expressed and has been studied in erythrocyte, kidney, brain and intestines. Interestingly, UT-B gene has been found more abundant in bladder than any other tissue. Recently, gene analyses demonstrate that SLC14A1 (UT-B) gene mutations are associated with bladder cancer, suggesting that urea transporter UT-B may play an important role in bladder carcinogenesis. In this study, we examined UT-B expression in bladder cancer with human primary bladder cancer tissues and cancer derived cell lines. Human UT-B has two isoforms. We found that normal bladder expresses long form of UT-B2 but was lost in 8 of 24 (33%) or significantly downregulated in 16 of 24 (67%) of primary bladder cancer patients. In contrast, the short form of UT-B1 lacking exon 3 was detected in 20 bladder cancer samples. Surprisingly, a 24-nt in-frame deletion in exon 4 in UT-B1 (UT-B1Δ24) was identified in 11 of 20 (55%) bladder tumors. This deletion caused a functional defect of UT-B1. Immunohistochemistry revealed that UT-B protein levels were significantly decreased in bladder cancers. Western blot analysis showed a weak UT-B band of 40 kDa in some tumors, consistent with UT-B1 gene expression detected by RT-PCR. Interestingly, bladder cancer associate UT-B1Δ24 was barely sialylated, reflecting impaired glycosylation of UT-B1 in bladder tumors. In conclusion, SLC14A1 gene and UT-B protein expression are significantly changed in bladder cancers. The aberrant UT-B expression may promote bladder cancer development or facilitate carcinogenesis induced by other carcinogens.

Copyright information:

© 2017 Hou, Alemozaffar, Yang, Sands, Kong and Chen.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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