{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chang X"],"funding":["Xi’an Science and Technology Planning Project Medical Research Project: General Research","Xi'an Science and Technology Planning Project Medical Research Project: General Research","General Project of Shaanxi Provincial Key Research and Development Plan - Social Development Field"],"pagination":["176"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9945719"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["Background
Hepatocellular carcinoma (HCC) is associated with a high occurrence, mortality, and poor prognosis. MLX interacting protein like (MLXIPL) is an important regulator of glucolipid metabolism and is involved in tumor progression. We aimed to clarify the role of MLXIPL in HCC and its underlying mechanisms.Methods
The level of MLXIPL was predicted using bioinformatic analysis and verified using quantitative real-time PCR (qPCR), immunohistochemical analysis, and western blot. We assessed the effects of MLXIPL on biological behaviors using the cell counting kit-8, colony formation, and Transwell assay. Glycolysis was evaluated using the Seahorse method. The interaction between MLXIPL and mechanistic target of rapamycin kinase (mTOR) was confirmed using RNA immunoprecip"],"journal":["BMC cancer"],"pubmed_title":["MLXIPL promotes the migration, invasion, and glycolysis of hepatocellular carcinoma cells by phosphorylation of mTOR."],"pmcid":["PMC9945719"],"funding_grant_id":["2023-YBSF-631","22YXYJ0134"],"pubmed_authors":["Yan P","Jia Y","Tian C","Cai Y","Chang X"],"additional_accession":[]},"is_claimable":false,"name":"MLXIPL promotes the migration, invasion, and glycolysis of hepatocellular carcinoma cells by phosphorylation of mTOR.","description":"Background
Hepatocellular carcinoma (HCC) is associated with a high occurrence, mortality, and poor prognosis. MLX interacting protein like (MLXIPL) is an important regulator of glucolipid metabolism and is involved in tumor progression. We aimed to clarify the role of MLXIPL in HCC and its underlying mechanisms.Methods
The level of MLXIPL was predicted using bioinformatic analysis and verified using quantitative real-time PCR (qPCR), immunohistochemical analysis, and western blot. We assessed the effects of MLXIPL on biological behaviors using the cell counting kit-8, colony formation, and Transwell assay. Glycolysis was evaluated using the Seahorse method. The interaction between MLXIPL and mechanistic target of rapamycin kinase (mTOR) was confirmed using RNA immunoprecip","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-19T00:55:50.902Z","creation":"2025-02-19T04:00:47.955Z"},"accession":"S-EPMC9945719","cross_references":{"pubmed":["36809979"],"doi":["10.1186/s12885-023-10652-5"]}}