{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen P"],"funding":["Fundo para o Desenvolvimento das Ciências e da Tecnologia (Science and Technology Development Fund)","Fundo para o Desenvolvimento das Ciências e da Tecnologia"],"pagination":["296"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9233710"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Gastric neuroendocrine carcinoma (GNEC) is a common type of neuroendocrine carcinoma (NEC) with a poor prognosis and limited therapeutic options. The underlying mechanisms of chemoresistance in patients with GNEC and those with NEC are largely unknown, and thus, reliable biomarkers and therapeutic targets that could improve treatment outcomes in patients with NECs are lacking. The aim of this study was to identify specific targets and investigate their roles in GNEC progression and treatment resistance. Differentially expressed genes (DEGs) were identified in GNEC specimens and were further analysed by focusing on their roles in chemoresistance. Gene Ontology (GO) and pathway enrichment analyses of GNEC DEGs revealed that synapse-related function was the most prominent cellular function pe"],"journal":["Cell death discovery"],"pubmed_title":["RUNDC3A regulates SNAP25-mediated chemotherapy resistance by binding AKT in gastric neuroendocrine carcinoma (GNEC)."],"pmcid":["PMC9233710"],"funding_grant_id":["0010/2021/AFJ","0055/2019/A1"],"pubmed_authors":["Zhang SD","Chen P","Li J","Wong SW","Wu Q","Kwok HF","Wang W","Lin Y"],"additional_accession":[]},"is_claimable":false,"name":"RUNDC3A regulates SNAP25-mediated chemotherapy resistance by binding AKT in gastric neuroendocrine carcinoma (GNEC).","description":"Gastric neuroendocrine carcinoma (GNEC) is a common type of neuroendocrine carcinoma (NEC) with a poor prognosis and limited therapeutic options. The underlying mechanisms of chemoresistance in patients with GNEC and those with NEC are largely unknown, and thus, reliable biomarkers and therapeutic targets that could improve treatment outcomes in patients with NECs are lacking. The aim of this study was to identify specific targets and investigate their roles in GNEC progression and treatment resistance. Differentially expressed genes (DEGs) were identified in GNEC specimens and were further analysed by focusing on their roles in chemoresistance. Gene Ontology (GO) and pathway enrichment analyses of GNEC DEGs revealed that synapse-related function was the most prominent cellular function pe","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2026-05-10T01:40:30.447Z","creation":"2024-11-19T17:22:41.52Z"},"accession":"S-EPMC9233710","cross_references":{"pubmed":["35752613"],"doi":["10.1038/s41420-022-01084-4"]}}