Metabolic Reprogramming Drives Pituitary Tumor Growth through Epigenetic Regulation of TERT

DOI Web Site 3 Citations 37 References
  • Onizuka Hiromi
    Department of Surgical Pathology, Tokyo Women’s Medical University Division of Pathological Neuroscience, Department of Pathology, Tokyo Women’s Medical University
  • Masui Kenta
    Division of Pathological Neuroscience, Department of Pathology, Tokyo Women’s Medical University
  • Amano Kosaku
    Department of Neurosurgery, Tokyo Women’s Medical University
  • Kawamata Takakazu
    Department of Neurosurgery, Tokyo Women’s Medical University
  • Yamamoto Tomoko
    Department of Surgical Pathology, Tokyo Women’s Medical University Division of Pathological Neuroscience, Department of Pathology, Tokyo Women’s Medical University
  • Nagashima Yoji
    Department of Surgical Pathology, Tokyo Women’s Medical University
  • Shibata Noriyuki
    Division of Pathological Neuroscience, Department of Pathology, Tokyo Women’s Medical University

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<p>Pituitary adenomas are common, benign brain tumors. Some tumors show aggressive phenotypes including early recurrence, local invasion and distant metastasis, but the underlying mechanism to drive the progression of pituitary tumors has remained to be clarified. Aerobic glycolysis known as the Warburg effect is one of the emerging hallmarks of cancer, which has an impact on the tumor biology partly through epigenetic regulation of the tumor-promoting genes. Here, we demonstrate metabolic reprogramming in pituitary tumors contributes to tumor cell growth with epigenetic changes such as histone acetylation. Notably, a shift in histone acetylation increases the expression of telomerase reverse transcriptase (TERT) oncogene, which drives metabolism-dependent cell proliferation in pituitary tumors. These indicate that epigenetic changes could be the specific biomarker for predicting the behavior of pituitary tumors and exploitable as a novel target for the aggressive types of the pituitary tumors.</p>

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