Abstract
Accumulating evidence suggests that the long noncoding RNAs (lncRNAs) urothelial cancer associated 1 (UCA1) and urothelial cancer associated 1α (UCA1α) play a critical role in the development and progression of bladder cancer. However, the detailed mechanism, in particular the role of the common region of UCA1 and UCA1α, termed UCA1 same sequence (USS, approximately 1265 bp), remains unknown. To address this, the full length of 1265 bp USS was obtained initially, and then produced pcDNA3.1(+)-based overexpression vectors and designed siRNAs for UCA1, UCA1α, and USS, and assessed their effects on the human bladder cancer cell lines UMUC3 (which does not express UCA1 and UCA1α) and 5637 (which has high expression of UCA1 and UCA1α), respectively. Overexpression of UCA1, UCA1α, and USS significantly increased bladder cancer cell proliferation and the number of S-phase cells, but significantly decreased cell apoptosis and the number of G0/G1 phase cells. Consistently, silencing UCA1 and USS significantly decreased bladder cancer cell proliferation and the number of S phase cells, but significantly increased apoptosis and the number of G0/G1 phase cells. These results suggest that USS, the common region of UCA1 and UCA1α, can promote bladder cancer tumorigenesis by increasing cell proliferation and decreasing cell apoptosis in a similar way to UCA1 and UCA1α lncRNAs. This not only transforms our understanding of the role of UCA1, UCA1α, and their common region in tumorigenesis, but may also provide a new target for future clinical applications.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.