http://purl.uniprot.org/citations/33141998 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/33141998 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundThe senescence of tumor cells is an important tumor suppressor mechanism. The present study aimed to investigate the role of long non-coding RNA (lncRNA) MEG3 (maternally expressed gene 3) in the senescence process of tumor cells and its potential molecular mechanism by competitively binding with microRNA miR-16-5p to regulate the expression of VGLL4 (encoding vestigial like family member 4).MethodsWe used etoposide to construct senescence models of tumor cells. The degree of cellular senescence was detected by senescence-associated β-galactosidase, cell cycle and senescence-associated secretory phenotype. The expression of lncRNA MEG3, miR-16-5p and VGLL4 in senescent or non-senescent cells was evaluated using a quantitative real-time reverse transcriptase-PCR (qRT-PCR) or western blotting. Dual luciferase reporter assays were used to detect the binding of miR-16-5p to lncRNA MEG3 and VGLL4. The mRNA and protein expression levels of senescence-related markers (p53, p21 and p16) were detected using qRT-PCR or western blotting.ResultsCompared to the control group, the expression of lncRNA MEG3 and VGLL4 was significantly up-regulated in senescent cells. Knockdown of lncRNA MEG3 and VGLL4 reduced the degree of senescence and the expression of p21 and p16. lncRNA MEG3 interfered with the expression of miR-16-5p in senescent A549 and MCF-7 cells. The expression of VGLL4 was regulated by miR-16-5p in senescent A549 and MCF-7 cells. lncRNA MEG3 participated in the senescent progress of tumor cells induced by etoposide via the miR-16-5p/VGLL4 axis.ConclusionsThe present study has confirmed the regulatory role of the lncRNA MEG3/miR-16-5p/VGLL4 axis in the low-dose etoposide-induced tumor cell senescence model, which has potential clinical application with respect to treating malignant tumors."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.org/dc/terms/identifier | "doi:10.1002/jgm.3291"xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Gao S."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Tao Y."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Wang B."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Meng X."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Miao Y."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Yue P."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/author | "Leng S.X."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/date | "2021"xsd:gYear |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/name | "J Gene Med"xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/pages | "e3291"xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/title | "The lncRNA MEG3/miR-16-5p/VGLL4 regulatory axis is involved in etoposide-induced senescence of tumor cells."xsd:string |
http://purl.uniprot.org/citations/33141998 | http://purl.uniprot.org/core/volume | "23"xsd:string |
http://purl.uniprot.org/citations/33141998 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/33141998 |
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http://purl.uniprot.org/uniprot/#_Q0H0I7-mappedCitation-33141998 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/33141998 |