ArticleMolecular biotechnology2022
Long Non-coding RNA CBR3 Antisense RNA 1 is Downregulated in Colorectal Cancer and Inhibits miR-29a-Mediated Cell Migration and Invasion.
Article in Molecular biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Epigenetic Alteration in Colorectal Cancer: Potential Diagnostic and Prognostic Implications.International journal of molecular sciences · 2024Review
- Assessment of salivary miRNA, clinical, and demographic characterization in colorectal cancer diagnosis.Translational oncology · 2024Article
- Trimetazidine Alleviates Bleomycin-Induced Pulmonary Fibrosis by Targeting the Long Noncoding RNA CBR3-AS1-Mediated miRNA-29 and Resistin-Like Molecule alpha 1: Deciphering a Novel Trifecta Role of LncRNA CBR3-AS1/miRNA-29/FIZZ1 Axis in Lung Fibrosis.Drug design, development and therapy · 2024Article
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although CBR3 Antisense RNA 1 (CBR3-AS1) has been characterized as an oncogenic long non-coding RNA (lncRNA) in several cancers, a recent study reported the downregulation of CBR3-AS1 in colorectal cancer (CRC). Therefore, we analyzed its role in CRC. CBR3-AS1 and microRNA-29a (miR-29a) expression in tissue samples from CRC patients were analyzed by RT-qPCR. The interaction between CBR3-AS1 and miR-29a was predicted by IntaRNA and validated by RNA pull-down assay. The location of CBR3-AS1 was analyzed by nuclear fractionation assay. CBR3-AS1 overexpression was performed to analyze its role in miR-29a expression. The roles of CBR3-AS1 and miR-29a in CRC cell migration and invasion were analyzed by Transwell assay. CBR3-AS1 was downregulated, and miR-29a was upregulated in CRC. CBR3-AS1 and miR-29a directly interacted with each other. CBR3-AS1 was localized in both nucleus and cytoplasm fractions. CBR3-AS1 overexpression failed to alter miR-29a expression but reduced its enhancing effects on cell invasion and migration. CBR3-AS1 is downregulated in CRC and inhibits miR-29a-mediated cell migration and invasion by sponging miR-29a.
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Registered trials
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