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http://purl.uniprot.org/citations/31773695http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31773695http://www.w3.org/2000/01/rdf-schema#comment"

Objective

To explore the possible role and mechanism of long non-coding ribonucleic acid LEF-AS1 (lncRNA LEF-AS1) in the pathogenesis of colorectal cancer (CRC).

Patients and methods

The expression levels of LEF-AS1 in 54 CRC tissue samples and adjacent normal ones were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). In the meantime, CRC cell lines were screened for subsequent in vitro experiments. LEF-AS1 siRNA was transfected into CRC cells using the liposome method. Then, cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assays were conducted to detect cell proliferation. Thereafter, transwell assay was performed to evaluate the cell migration capacity, as well as invasiveness, Caspase-3 activity was examined to estimate cell apoptosis, and flow cytometry was applied for cell cycle detection. Subsequently, bioinformatics analysis was carried out to predict the target genes of micro RNA (miR)-505 that were predicted to be able to bind to LEF-AS1, while the relative activity of luciferase between miR-505 and KIF3B or LEF-AS1 was examined via luciferase gene reporter assay. In addition, the interaction between KIF3B and miR-505, as well as LEF-AS1, was further verified by RNA knockdown assay and cell reversal experiments.

Results

The expression of LEF-AS1 in CRC tissue specimens was found to be markedly higher than that in normal colon tissues. After transfection with LEF-AS1 siRNA, the cell viability, as well as cell migration and invasion capacities, were both attenuated. However, the cell apoptosis rate was conversely elevated. Dual-Luciferase reporter assay revealed that LEF-AS1 could combine with miR-505, which was capable of targeted binding to KIF3B. In addition, LEF-AS1 siRNA transfection attenuated cell proliferation, migration, and invasion capacities, which could be partially reversed by the overexpression of KIF3B.

Conclusions

In this research, LEF-AS1 is highly expressed in CRC tissues and cell lines. However, the down-regulation of LEF-AS1 reduces the proliferation rate and suppresses the invasiveness and metastasis of CRC cells through the LEF-AS1/miR-505/KIF3B axis."xsd:string
http://purl.uniprot.org/citations/31773695http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_201911_19429"xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/author"Huang A.L."xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/author"Gong X.Y."xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/pages"9362-9370"xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/title"LEF-AS1 participates in occurrence of colorectal cancer through adsorbing miR-505 and promoting KIF3B expression."xsd:string
http://purl.uniprot.org/citations/31773695http://purl.uniprot.org/core/volume"23"xsd:string
http://purl.uniprot.org/citations/31773695http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31773695
http://purl.uniprot.org/citations/31773695http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31773695
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http://purl.uniprot.org/uniprot/#_O15066-mappedCitation-31773695http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31773695
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http://purl.uniprot.org/uniprot/O15066http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31773695