| http://purl.uniprot.org/citations/35278461 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35278461 | http://www.w3.org/2000/01/rdf-schema#comment | "Several studies have demonstrated that B7-H4 is highly expressed in a variety of cancers and often affects tumor development. However, its role in cancer stemness and epithelial-to-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) has not been reported. Here, we investigated the relationship between B7-H4 expression and cancer stemness and EMT by immunohistochemistry in 106 NSCLC tissues obtained from patients. The results confirmed that B7-H4 is highly expressed in NSCLC tissues and closely correlated with the expression of EMT-related proteins (Snail, Vimentin) and cancer stemness-related proteins (SOX2, SOX9, and CD44). Immunofluorescence assay indicated that B7-H4 colocalized with SOX2 and SOX9 in the nuclei of NSCLC cells. Additionally, upon knocking down B7-H4, the expression of SOX2, SOX9, and CD44, as well as of Snail and Vimentin was inhibited, whereas E-cadherin expression was enhanced in NSCLC cells. Meanwhile, inhibiting the expression of B7-H4 resulted in reduced invasion and migration ability of NSCLC cells. Mechanistically, silencing B7-H4 activated the adenosine monophosphate-activated protein kinase /mammalian target of rapamycin signaling, which in turn, negatively regulated cell proliferation, stemness, and migration. In conclusion, our results suggest that B7-H4 expression is high in NSCLC tissues, and it has an effect on EMT and cancer stemness. This further suggests that B7-H4 has a potential role in promoting the progression of NSCLC and thereby could be a potential therapeutic target in NSCLC treatment."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.yexmp.2022.104755"xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Feng Y."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Jin Y."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Li M."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Piao L."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Xuan Y."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/author | "Che N."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/name | "Exp Mol Pathol"xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/pages | "104755"xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/title | "B7-H4 expression promotes non-small cell lung cancer progression via AMPK/mTOR signaling."xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://purl.uniprot.org/core/volume | "125"xsd:string |
| http://purl.uniprot.org/citations/35278461 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35278461 |
| http://purl.uniprot.org/citations/35278461 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/35278461 |
| http://purl.uniprot.org/uniprot/#_Q7Z7D3-mappedCitation-35278461 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/35278461 |
| http://purl.uniprot.org/uniprot/Q7Z7D3 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/35278461 |