Downregulation of c-MYC Protein Levels Contributes to Cancer Cell Survival under Dual Deficiency of Oxygen and Glucose

We show that c-MYC protein levels in cancer cells are strikingly reduced in the area distant from the blood vessels in vivo and under oxygen- and glucosedeprived conditions in vitro

Hiroaki Okuyama; Hiroko Endo; Tamaki Akashika; Kikuya Kato; Masahiro Inoue


Scholarcy highlights

  • Most solid tumors contain substantially large hypoxic regions
  • To evaluate the proliferation and metabolic activity of cancer cells located in the hypoxic region of the tumor, we examined xenograft tumors derived from the human colon cancer cell line, HCT116
  • Phosphorylated S6, downstream of mTOR and involved in ribosomal biogenesis, was detected only in the area proximal to the tumor vessels but not in the area distant from the tumor vessels. These results indicate that cancer cells proximal to the blood vessels are active in proliferation and metabolism, whereas cancer cells distant from the blood vessels are inactive
  • We showed that c-MYC levels were downregulated in regions distant from blood vessels in solid tumors derived from a colon cancer cell line, HCT116
  • Downregulation of c-MYC protein contributes to survival of cancer cells under the dual-deprivation conditions, as the forced reduction of c-MYC expression by short hairpin RNA reduced necrotic cell death under these conditions
  • Tumor hypoxia is strongly associated with malignant progression, poor prognosis, and resistance to chemotherapy and radiation
  • We speculate on this subject as follows: Given that c-MYC stimulates energyconsuming processes, rapid depletion of ATP levels resulting from activation of c-MYC under dual-deprivation conditions might drive the cancer cells to necrosis

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