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. 2015 Apr 20;125(5):2109–2122. doi: 10.1172/JCI79134

Figure 7. Graphical model.

Figure 7

TERT levels, which limit the reconstitution of telomerase activity in normal cells, are upregulated by increased MYC in cancer cells. TERT, in turn, enhances MYC stability and function, thereby regulating its own levels and telomerase activity. This function of TERT does not require Terc and is independent of its function at telomeres. Enhanced MYC stability and function in high-TERT and high-MYC cells, a consequence of this feed-forward mechanism, lead to enhanced oncogenesis due to downstream targets of MYC, which are known to regulate aspects of cell cycle, proliferation, and metabolism.