Metabolic Reprogramming by Malat1 Depletion in Prostate Cancer.

摘要: The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) promotes growth and progression in prostate cancer (PCa); however, little is known about its possible impact PCa metabolism. aim of this work has been the assessment metabolic reprogramming associated with MALAT1 silencing human cells an ex vivo model organotypic slice cultures (OSCs). Cultured OSCs derived from primary tumors were transfected specific gapmers. Cell survival, gene profiling, evaluation targeted metabolites enzymes assessed. Computational analysis was made considering expression changes occurring markers following targeting cultured OSCs. reduced some enzymes, including malic enzyme 3, pyruvate dehydrogenase kinases choline kinase A. Consequently, metabolism switched toward a glycolytic phenotype characterized by increased lactate production paralleled arrest cell death. Conversely, function mitochondrial succinate oxidative phosphorylation markedly reduced. A similar effect observed Based on this, predictive algorithm developed aimed to predict tumor recurrence subset patients. gapmer delivery restored normal energy pathway