{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang L"],"funding":["National Natural Science Foundation of China-Guangdong Joint Fund","Guangxi Zhuang Autonomous Region Health and Family Planning Commission","National Natural Science Foundation of China"],"pagination":["e12981"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7941240"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(3)"],"pubmed_abstract":["<h4>Objectives</h4>Circular RNAs (circRNAs) are essential participants in tumour progression. This study focused on investigating the mechanism of a novel functional circRNA in gastric cancer (GC).<h4>Methods</h4>Gene expression was detected by qRT-PCR or Western blot. Survival curves were generated via Kaplan-Meier method. In vitro and in vivo assays were used to investigate the impact of circ_SMAD4 on GC cell growth and tumorigenesis. Agarose gel electrophoresis assay, RNase R treatment and Sanger sequencing were utilized for confirming the circular structure of circ_SMAD4. Relationship between molecules was monitored by a series of mechanical experiments, as needed.<h4>Results</h4>Circ_SMAD4 expression was potentiated in GC. Circ_SMAD4 depletion impeded GC cell growth in vitro and restrained tumorigenesis in vivo. Mechanically, nuclear circ_SMAD4 recruited TCF4 to facilitate CTNNB1 transcription, while cytoplasmic circ_SMAD4 sequestered miR-1276 to prevent the silence of CTNNB1 mRNA, leading to activation of Wnt/β-catenin pathway. Rescue experiments validated that circ_SMAD4 depended on miR-1276/TCF4-regulated CTNNB1 to elicit accelerating effects on GC cell growth.<h4>Conclusion</h4>Circ_SMAD4 facilitated GC tumorigenesis by activating CTNNB1-dependent Wnt/β-catenin pathway. Hopefully, the findings could provide new clues for improving GC prognosis and treatment."],"journal":["Cell proliferation"],"pubmed_title":["Circ_SMAD4 promotes gastric carcinogenesis by activating wnt/β-catenin pathway."],"pmcid":["PMC7941240"],"funding_grant_id":["S201407‐04","81560402","S201407-04"],"pubmed_authors":["Yi X","Ma L","Xiao X","Zheng Q","Li B","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"Circ_SMAD4 promotes gastric carcinogenesis by activating wnt/β-catenin pathway.","description":"<h4>Objectives</h4>Circular RNAs (circRNAs) are essential participants in tumour progression. This study focused on investigating the mechanism of a novel functional circRNA in gastric cancer (GC).<h4>Methods</h4>Gene expression was detected by qRT-PCR or Western blot. Survival curves were generated via Kaplan-Meier method. In vitro and in vivo assays were used to investigate the impact of circ_SMAD4 on GC cell growth and tumorigenesis. Agarose gel electrophoresis assay, RNase R treatment and Sanger sequencing were utilized for confirming the circular structure of circ_SMAD4. Relationship between molecules was monitored by a series of mechanical experiments, as needed.<h4>Results</h4>Circ_SMAD4 expression was potentiated in GC. Circ_SMAD4 depletion impeded GC cell growth in vitro and restrained tumorigenesis in vivo. Mechanically, nuclear circ_SMAD4 recruited TCF4 to facilitate CTNNB1 transcription, while cytoplasmic circ_SMAD4 sequestered miR-1276 to prevent the silence of CTNNB1 mRNA, leading to activation of Wnt/β-catenin pathway. Rescue experiments validated that circ_SMAD4 depended on miR-1276/TCF4-regulated CTNNB1 to elicit accelerating effects on GC cell growth.<h4>Conclusion</h4>Circ_SMAD4 facilitated GC tumorigenesis by activating CTNNB1-dependent Wnt/β-catenin pathway. Hopefully, the findings could provide new clues for improving GC prognosis and treatment.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-18T13:42:27.688Z","creation":"2025-04-06T23:28:24.811Z"},"accession":"S-EPMC7941240","cross_references":{"pubmed":["33458917"],"doi":["10.1111/cpr.12981"]}}