The study investigates the role of c-Myc in regulating mitochondrial glutaminase (GLS) expression and glutamine metabolism in cancer cells. c-Myc, an oncogenic transcription factor, represses miR-23a and miR-23b, leading to increased GLS expression. This results in enhanced glutamine catabolism, which is crucial for cell proliferation and energy production. The authors used human P-493 B cells and PC3 prostate cancer cells to demonstrate that reduced Myc expression leads to decreased GLS levels, impaired cell proliferation, and increased reactive oxygen species (ROS). They also found that GLS is directly regulated by miR-23a and miR-23b, which target the 3'UTR of the GLS gene. The study highlights a novel pathway where c-Myc suppression of miR-23 enhances glutamine metabolism, providing insights into the regulation of tumor metabolism and energy homeostasis.The study investigates the role of c-Myc in regulating mitochondrial glutaminase (GLS) expression and glutamine metabolism in cancer cells. c-Myc, an oncogenic transcription factor, represses miR-23a and miR-23b, leading to increased GLS expression. This results in enhanced glutamine catabolism, which is crucial for cell proliferation and energy production. The authors used human P-493 B cells and PC3 prostate cancer cells to demonstrate that reduced Myc expression leads to decreased GLS levels, impaired cell proliferation, and increased reactive oxygen species (ROS). They also found that GLS is directly regulated by miR-23a and miR-23b, which target the 3'UTR of the GLS gene. The study highlights a novel pathway where c-Myc suppression of miR-23 enhances glutamine metabolism, providing insights into the regulation of tumor metabolism and energy homeostasis.