Abstract
Overwhelming evidence has suggested that dysregulated long noncoding RNAs (lncRNAs) play a critical modulating effect in the evolution of breast cancer (BRCA). Nevertheless, the roles of lncRNA PTPRG antisense RNA 1 (PTPRG-AS1) in BRCA and the underlying mechanisms have not been experimentally validated and functionally annotated. The expression of lncRNA PTPRG-AS1 in BRCA tissues and cell lines was evaluated by reverse transcription-quantitative PCR (RT-qPCR), and by using public databases. The proliferation of BRCA cells was detected using Cell Counting Kit-8 and colony formation assays. Wound healing assay, and Transwell migration and invasion assays were carried out to explore the migratory and invasive abilities of BRCA cells. The interaction between lncRNA PTPRG-AS1, microRNA (miR)-4659a-3p and glutaminyl-peptide cyclotransferase (QPCT) was verified using RT-qPCR, dual-luciferase reporter assay and Western blotting. The results showed that LncRNA PTPRG-AS1 was markedly upregulated in BRCA tissues and cell lines. Knocking down lncRNA PTPRG-AS1 significantly inhibited the proliferation, migration and invasion of BRCA cells, while overexpression of lncRNA PTPRG-AS1 enhanced the aforementioned properties of BRCA cells. Further analyses revealed that PTPRG-AS1 may act as a molecular sponge for miR-4659a-3p, thus regulating QPCT expression, therefore, acting as an oncogene in BRCA. Collectively, the study demonstrates that lncRNA PTPRG-AS1 may act as a competing endogenous RNA by regulating the miR-4659a-3p/QPCT axis in BRCA progression. This lncRNA could potentially be a biomarker and therapeutic target for BRCA.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
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.