| http://purl.uniprot.org/citations/37884580 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/37884580 | http://www.w3.org/2000/01/rdf-schema#comment | "Non-small cell lung cancer (NSCLC) is a common and lethal malignancy. The carcinogenic roles of lncRNA CALML3 antisense RNA 1 (CALML3-AS1) have been documented. However, the function and potential mechanisms of CALML3-AS1 in the progression of NSCLC need to be further explored. The molecule expression was assessed by qRT-PCR and Western blot. The subcellular localization of CALML3-AS1 was observed by fluorescence in situ hybridization (FISH). The malignant behaviors of NSCLC cells were evaluated by CCK-8, colony formation, EdU, wound healing and transwell assays. In vivo xenograft tumor and liver metastatic models were established. The molecular mechanisms were investigated by RIP, RNA pull-down and ChIP assays. The methylation level was detected by MSP. Herein, we found that CALML3-AS1 was upregulated, while butyrophilin-like 9 (BTNL9) was downregulated in NSCLC. Functionally, CALML3-AS1 depletion repressed NSCLC cell malignant phenotypes, in vivo tumor growth, and liver metastasis. Mechanistically, AlkB homolog 5 (ALKBH5) enhanced CALML3-AS1 stability via N6-methyladenosine (m6A) demethylation, whereas m6A reader YTH domain-containing 2 (YTHDC2) destabilized CALML3-AS1. Moreover, CALML3-AS1 inhibited BTNL9 transcription and expression through the recruitment of Zeste homolog 2 (EZH2). Rescue experiments demonstrated that BTNL9 downregulation counteracted sh-CALML3-AS1-mediated antitumor effects on NSCLC. Taken together, CALML3-AS1 modulated by ALKBH5 and YTHDC2 in an m6A modification dependent manner drives NSCLC progression via epigenetically repressing BTNL9."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41417-023-00670-7"xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Lin H."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Li L.F."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Zhang H."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Wang S.Q."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Duan C.J."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Zhang C.F."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Zhu J.B."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Wang L.N."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/author | "Cheng Y.D."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/name | "Cancer Gene Ther"xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/pages | "1649-1662"xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/title | "LncRNA CALML3-AS1 modulated by m6A modification induces BTNL9 methylation to drive non-small-cell lung cancer progression."xsd:string |
| http://purl.uniprot.org/citations/37884580 | http://purl.uniprot.org/core/volume | "30"xsd:string |
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