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Author Xie, Hua ♦ Zhu, Dongmei ♦ Xu, Cao ♦ Zhu, Hairong ♦ Chen, Pingfa ♦ Li, Hongxing ♦ Liu, Xiang ♦ Xia, Yankai ♦ Tang, Weibing
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANIMAL TISSUES ♦ APOPTOSIS ♦ CELL CYCLE ♦ COMPARATIVE EVALUATIONS ♦ DESIGN ♦ DISEASES ♦ GENES ♦ HUMAN POPULATIONS ♦ LARGE INTESTINE ♦ MESSENGER-RNA ♦ PATHOGENESIS ♦ PATIENTS ♦ PEDIATRICS ♦ PHENOTYPE ♦ POLYMERASE CHAIN REACTION ♦ PROTEINS ♦ VIABILITY
Abstract Long noncoding RNAs (lncRNAs) have been confirmed to be associated with various human diseases. However, whether they are associated with Hirschsprung disease (HSCR) progression remains unclear. In this study, we designed the experiment to explore the relationship between lncRNA HOTTIP and HOXA13, and their pathogenicity to HSCR. Quantitative real-time PCR and Western blot were performed to detect the levels of lncRNA, mRNAs, and proteins in colon tissues from 79 patients with HSCR and 79 controls. Small RNA interference transfection was used to study the function experiments in human 293T and SK-N-BE cell lines. The cell viability and activities were detected by the transwell assays, CCK8 assay, and flow cytometry, respectively. LncRNA HOTTIP and HOXA13 were significantly down-regulated in HSCR compared to the controls. Meanwhile, the declined extent of their expression levels makes sense between two main phenotype of HSCR. SiRNA-mediated knock-down of HOTTIP or HOXA13 correlated with decreased levels of each other and both reduced the cell migration and proliferation without affecting cell apoptosis or cell cycle. Our study demonstrates that aberrant reduction of HOTTIP and HOXA13, which have a bidirectional regulatory loop, may play an important role in the pathogenesis of HSCR. - Highlights: • LncRNA HOTTIP and HOXA13 are both down-regulated in HSCR. • HOTTIP and HOXA13 can regulate each other in 293T and SK-N-BE(2) cell lines. • Both HOTTIP and HOXA13 can decrease cell migration and proliferation.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-08-07
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 463
Issue Number 4


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