{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li J"],"funding":["National Natural Science Foundation of China"],"pagination":["259-272"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8986754"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(2)"],"pubmed_abstract":["Stanniocalcin-2 (STC2) has been proved to regulate a variety of signaling pathways including cell growth, metastasis, and therapeutic resistance. However, the role of STC2 in the regulation of nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, we investigated the regulatory function of STC2 on epithelial-mesenchymal transition (EMT) and glycolysis traits in NPC and revealed the underlying molecular mechanisms. We found that STC2 was highly expressed in primary nasopharyngeal carcinoma tissues and lymph node metastatic tissues. Silencing of STC2 inhibited cell proliferation, invasion, and glycolysis. Further analyses for the clinical samples demonstrated that STC2 expression was associated with the poor clinical progression. Moreover, we demonstrated the interaction of"],"journal":["Cell biology and toxicology"],"pubmed_title":["Stanniocalcin-2 promotes cell EMT and glycolysis via activating ITGB2/FAK/SOX6 signaling pathway in nasopharyngeal carcinoma."],"pmcid":["PMC8986754"],"funding_grant_id":["81872117"],"pubmed_authors":["Li J","Shen Z","Xu M","Zhang Z","Feng X","Bu F","Zhang X","Tan C","Wang Z","Sun J"],"additional_accession":[]},"is_claimable":false,"name":"Stanniocalcin-2 promotes cell EMT and glycolysis via activating ITGB2/FAK/SOX6 signaling pathway in nasopharyngeal carcinoma.","description":"Stanniocalcin-2 (STC2) has been proved to regulate a variety of signaling pathways including cell growth, metastasis, and therapeutic resistance. However, the role of STC2 in the regulation of nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, we investigated the regulatory function of STC2 on epithelial-mesenchymal transition (EMT) and glycolysis traits in NPC and revealed the underlying molecular mechanisms. We found that STC2 was highly expressed in primary nasopharyngeal carcinoma tissues and lymph node metastatic tissues. Silencing of STC2 inhibited cell proliferation, invasion, and glycolysis. Further analyses for the clinical samples demonstrated that STC2 expression was associated with the poor clinical progression. Moreover, we demonstrated the interaction of","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-06-01T12:11:14.605Z","creation":"2025-06-01T12:11:14.605Z"},"accession":"S-EPMC8986754","cross_references":{"pubmed":["33797657"],"doi":["10.1007/s10565-021-09600-5"]}}