{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":67,"searchCount":0},"additional":{"submitter":["Zhang Q"],"funding":["the Natural Science Foundationof Henan Province","Key R&D and Promotion Projects in Henan Province","the Key Scientific Research Projects of Henan Higher Education Institutions"],"pagination":["8206-8220"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7348145"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(14)"],"pubmed_abstract":["Long non-coding RNAs (lncRNAs) widely participate in ESCC development and progression; however, the prognostic factors and therapeutic strategies implicated in ESCC development and progression remain to be under investigation. The purpose of the current study was to explore whether WDFY3-AS2 may be a potential prognostic factor and investigate its biological functions in ESCC. Here, WDFY3-AS2 was frequently down-regulated in ESCC tissues and cells, and its expression was correlated with TNM stage, lymph node metastasis and poor prognosis of ESCC patients. Moreover, WDFY3-AS2 down-regulation significantly promoted cell proliferation and invasion, whereas WDFY3-AS2 up-regulation markedly suppressed cell proliferation and invasion in ESCC EC9706 and TE1 cells, coupled with EMT phenotype alterations. WDFY3-AS2 functioned as a competing endogenous RNA (ceRNA) for sponging miR-2355-5p, further resulted in the up-regulation of its target gene SOCS2, followed by suppression of JAK2/Stat5 signalling pathway, to suppress ESCC cell proliferation and invasion in EC9706 and TE1 cells. These findings suggest that WDFY3-AS2 may participate in ESCC development and progression, and may be a novel prognostic factor for ESCC patients, and thus targeting WDFY3-AS2/miR-2355-5p/SOCS2 signalling axis may be a novel therapeutic strategy for ESCC patients."],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["LncRNA WDFY3-AS2 suppresses proliferation and invasion in oesophageal squamous cell carcinoma by regulating miR-2355-5p/SOCS2 axis."],"pmcid":["PMC7348145"],"funding_grant_id":["182300410377","182102310380","17A180016"],"pubmed_authors":["Liu H","Ma S","Li S","Zhang Y","Guan F","Guo W","Zhang Q","Fan T"],"view_count":["67"],"additional_accession":[]},"is_claimable":false,"name":"LncRNA WDFY3-AS2 suppresses proliferation and invasion in oesophageal squamous cell carcinoma by regulating miR-2355-5p/SOCS2 axis.","description":"Long non-coding RNAs (lncRNAs) widely participate in ESCC development and progression; however, the prognostic factors and therapeutic strategies implicated in ESCC development and progression remain to be under investigation. The purpose of the current study was to explore whether WDFY3-AS2 may be a potential prognostic factor and investigate its biological functions in ESCC. Here, WDFY3-AS2 was frequently down-regulated in ESCC tissues and cells, and its expression was correlated with TNM stage, lymph node metastasis and poor prognosis of ESCC patients. Moreover, WDFY3-AS2 down-regulation significantly promoted cell proliferation and invasion, whereas WDFY3-AS2 up-regulation markedly suppressed cell proliferation and invasion in ESCC EC9706 and TE1 cells, coupled with EMT phenotype alterations. WDFY3-AS2 functioned as a competing endogenous RNA (ceRNA) for sponging miR-2355-5p, further resulted in the up-regulation of its target gene SOCS2, followed by suppression of JAK2/Stat5 signalling pathway, to suppress ESCC cell proliferation and invasion in EC9706 and TE1 cells. These findings suggest that WDFY3-AS2 may participate in ESCC development and progression, and may be a novel prognostic factor for ESCC patients, and thus targeting WDFY3-AS2/miR-2355-5p/SOCS2 signalling axis may be a novel therapeutic strategy for ESCC patients.","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jul","modification":"2021-02-20T02:04:23Z","creation":"2020-10-29T08:38:49Z"},"accession":"S-EPMC7348145","cross_references":{"pubmed":["32536038"],"doi":["10.1111/jcmm.15488"]}}