biostudies-literatureUnknown57(7)Chen QMitochondrial dysfunction is implicated in numerous disorders, including type 2 diabetes, Alzheimer's disease and cancer. Long non-coding RNAs (lncRNAs) are emerging as pivotal regulators of cellular energy metabolism, yet their roles remain largely unclear. In this study, we identify an lncRNA named linc-PMB, which is associated with mTOR and promotes mitochondrial biogenesis, through microarray analysis. We demonstrate that the knockdown of <i>linc-PMB</i> results in significantly impaired mitochondrial respiration and biogenesis, along with altered expressions of related genes. Conversely, overexpression of linc-PMB markedly increases mitochondrial function. We further reveal that linc-PMB interacts with the RNA-binding protein HuR, promoting the stabilization of SIRT1 mRNA and a substaActa biochimica et biophysica Sinica1057-1067https://www.ebi.ac.uk/biostudies/studies/S-EPMC12367985biostudies-literaturemTOR-related linc-PMB promotes mitochondrial biogenesis via stabilizing SIRT1 mRNA through binding to the HuR protein.PMC12367985Liu YChen QYu MWang SZhang HWang DLiao WCai YfalsemTOR-related linc-PMB promotes mitochondrial biogenesis via stabilizing SIRT1 mRNA through binding to the HuR protein.Mitochondrial dysfunction is implicated in numerous disorders, including type 2 diabetes, Alzheimer's disease and cancer. Long non-coding RNAs (lncRNAs) are emerging as pivotal regulators of cellular energy metabolism, yet their roles remain largely unclear. In this study, we identify an lncRNA named linc-PMB, which is associated with mTOR and promotes mitochondrial biogenesis, through microarray analysis. We demonstrate that the knockdown of <i>linc-PMB</i> results in significantly impaired mitochondrial respiration and biogenesis, along with altered expressions of related genes. Conversely, overexpression of linc-PMB markedly increases mitochondrial function. We further reveal that linc-PMB interacts with the RNA-binding protein HuR, promoting the stabilization of SIRT1 mRNA and a substa2025-01-01T00:00:00Z2025 Jan2026-05-05T19:00:35.539Z2026-04-07T21:50:13.886ZS-EPMC123679853991097710.3724/abbs.2024236