{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["21"],"submitter":["Liu S"],"funding":["METAvivor"],"pubmed_abstract":["Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows promising antitumor activity in preclinical studies. However, the efficacy of recombinant TRAIL in clinical trials is compromised by its short serum half-life and low <i>in vivo</i> stability. Induction of endogenous TRAIL may overcome the limitations and become a new strategy for cancer treatment. Here, we discovered that metformin increased TRAIL expression and induced apoptosis in triple-negative breast cancer (TNBC) and non-small cell lung cancer (NSCLC) cells. Metformin did not alter the expression of TRAIL receptors (TRAIL-R1/DR4 and TRAIL-R2/DR5). Metformin-upregulated TRAIL was secreted into conditioned medium (CM) and found to be functional, since the CM promoted TNBC cells undergoing apoptosis, which was abroga"],"journal":["Molecular therapy oncolytics"],"pagination":["303-314"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8167201"],"repository":["biostudies-literature"],"pubmed_title":["Upregulation of endogenous TRAIL-elicited apoptosis is essential for metformin-mediated antitumor activity against TNBC and NSCLC."],"pmcid":["PMC8167201"],"pubmed_authors":["Liu H","Zhou L","He Z","Lyu H","Ruan S","Hou D","Liu B","Liu S","Polsdofer EV","Thor AD"],"additional_accession":[]},"is_claimable":false,"name":"Upregulation of endogenous TRAIL-elicited apoptosis is essential for metformin-mediated antitumor activity against TNBC and NSCLC.","description":"Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) shows promising antitumor activity in preclinical studies. However, the efficacy of recombinant TRAIL in clinical trials is compromised by its short serum half-life and low <i>in vivo</i> stability. Induction of endogenous TRAIL may overcome the limitations and become a new strategy for cancer treatment. Here, we discovered that metformin increased TRAIL expression and induced apoptosis in triple-negative breast cancer (TNBC) and non-small cell lung cancer (NSCLC) cells. Metformin did not alter the expression of TRAIL receptors (TRAIL-R1/DR4 and TRAIL-R2/DR5). Metformin-upregulated TRAIL was secreted into conditioned medium (CM) and found to be functional, since the CM promoted TNBC cells undergoing apoptosis, which was abroga","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2025-06-01T02:01:57.345Z","creation":"2025-06-01T02:01:57.345Z"},"accession":"S-EPMC8167201","cross_references":{"pubmed":["34141868"],"doi":["10.1016/j.omto.2021.04.012"]}}