ArticleBioengineered2022
LncRNA ubiquitin-binding protein domain protein 10 antisense RNA 1 inhibits colon adenocarcinoma progression via the miR-515-5p/slit guidance ligand 3 axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Development of a prognostic risk model for predicting biochemical recurrence-free survival in patients with prostate cancer based on lysine acetylation.Translational andrology and urology · 2025Article
- Prospect of extracellular vesicles in tumor immunotherapy.Frontiers in immunology · 2025Review
- Exploring the role of ubiquitin regulatory X domain family proteins in cancers: bioinformatics insights, mechanisms, and implications for therapy.Journal of translational medicine · 2024Review
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- SLIT3 deficiency promotes non-small cell lung cancer progression by modulating UBE2C/WNT signaling.Open life sciences · 2024Article
- Identification and validation of an immune-related lncRNAs signature to predict the overall survival of ovarian cancer.Frontiers in oncology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated long non-coding RNAs (lncRNAs) play an important role in cancer progression. However, there have been limited reports to date of the involvement of ubiquitin-binding protein domain protein 10 antisense RNA 1 (UBXN10-AS1) in cancer. Our aim was to explore the role and underlying mechanism of UBXN10-AS1 in the occurrence of colon adenocarcinoma (COAD). Real-time quantitative PCR and Western blotting were performed to determine the expression of UBXN10-AS1, miR-515-5p, and Slit guidance ligand 3 (SLIT3). Cell Counting Kit-8 and wound healing scratch assays were performed to measure COAD cell proliferation and migration. A xenograft assay was performed to examine tumor growth in vivo. Luciferase reporter and RNA immunoprecipitation (RIP) assays were used to determine the binding interaction among miR-515-5p, UBXN10-AS1, and SLIT3. The results showed that UBXN10-AS1 and SLIT3 were expressed at low levels in COAD tissues, while miR-515-5p was expressed at high levels. UBXN10-AS1 overexpression suppressed tumor growth in vitro and in vivo. The luciferase reporter and RNA RIP assays demonstrated that UBXN10-AS1 targeted miR-515-5p, which in turn targeted SLIT3. Functionally, miR-515-5p overexpression reversed the inhibition of COAD cell proliferation and migration by UBXN10-AS1 overexpression, and SLIT3 overexpression counteracted the oncogenicity of miR-515-5p. Our study shows that UBXN10-AS1 modulates the miR-515-5p/SLIT3 axis, thereby resulting in the inhibition of COAD cell proliferation and migration.
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