http://purl.uniprot.org/citations/35076836 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/35076836 | http://www.w3.org/2000/01/rdf-schema#comment | "Mounting evidence indicates that lncRNAs (long noncoding RNAs) are involved in the initiation and development of tumors, including non-small cell lung cancer (NSCLC). However, the involvement of C-terminal binding protein-antisense RNA 2 (CTBP1-AS2) in NSCLC remains to be studied. RT-qPCR was carried out to detect CTBP1-AS2 and miR-623 expression in NSCLC cells and tissues. CCK-8 and flow cytometry were performed to measure cell proliferation and cell cycle progression. Luciferase reporter analysis was performed to study the potential target of CTBP1-AS2. We found that CTBP1-AS2 expression was upregulated in NSCLC cells (SPC-A1, A549, H23, and H1299) compared to 16HBE cells. We demonstrated that the CTBP1-AS2 level was higher in NSCLC specimens than in paired non-tumor specimens. Elevated expression of CTBP1-AS2 increased cell growth and induced cell cycle progression and epithelial-mesenchymal transition (EMT). We also found that ectopic expression of CTBP1-AS2 inhibited miR-623 expression. MMP3 was a direct target of miR-623, and luciferase reporter assays suggested that miR-623 overexpression suppressed the luciferase expression driven by the MMP3 wild-type reporter but not the mutant reporter. Overexpression of miR-623 suppressed MMP3 expression in A549 cells, and overexpression of CTBP1-AS2 increased MMP3 expression in A549 cells. Moreover, the miR-623 level was lower in NSCLC specimens than in paired non-tumor specimens, and CTBP1-AS2 expression was negatively correlated with miR-623 expression in NSCLC samples. Furthermore, overexpression of CTBP1-AS2 enhanced cell growth, cell cycle progression, and EMT progression by modulating MMP3 expression."xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.org/dc/terms/identifier | "doi:10.1007/s11356-021-15921-z"xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/author | "Yang G."xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/author | "Zhang C."xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/name | "Environ Sci Pollut Res Int"xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/pages | "38385-38394"xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/title | "CTBP1-AS2 promoted non-small cell lung cancer progression via sponging the miR-623/MMP3 axis."xsd:string |
http://purl.uniprot.org/citations/35076836 | http://purl.uniprot.org/core/volume | "29"xsd:string |
http://purl.uniprot.org/citations/35076836 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35076836 |
http://purl.uniprot.org/citations/35076836 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/35076836 |
http://purl.uniprot.org/uniprot/#_Q4W5N5-mappedCitation-35076836 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35076836 |
http://purl.uniprot.org/uniprot/#_Q96CW7-mappedCitation-35076836 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35076836 |
http://purl.uniprot.org/uniprot/Q96CW7 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/35076836 |
http://purl.uniprot.org/uniprot/Q4W5N5 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/35076836 |