biostudies-literatureWu QThe Research Fund of Shanghai Tongren Hospital, Shanghai Jiaotong University School of MedicineShanghai Municipal Health CommissionNational Natural Science Foundation of ChinaShanghai Municipal Health Bureau Key Disciplines GrantNatural Science Foundation of the Science and Technology Commission of Shanghai Municipality1258-1278https://www.ebi.ac.uk/biostudies/studies/S-EPMC7934455biostudies-literatureUnknown29(3)Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNMolecular therapy : the journal of the American Society of Gene TherapylncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.PMC7934455ZK2015A2415411971000815705498147224220194Y0373TRYJ20151116411972700TRYJ201613Shi MWu QMa JWei JWang YMeng WfalselncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SN2021-01-01T00:00:00Z2021 Mar2025-05-18T12:54:39.479Z2025-05-18T12:54:39.479ZS-EPMC79344553306877810.1016/j.ymthe.2020.10.011