Abstract
Telomerase elongates telomeres and is crucial for maintaining genomic stability. While stem cells and cancer cells display high telomerase activity, normal somatic cells lack telomerase activity primarily due to transcriptional repression of telomerase reverse transcriptase (TERT), the catalytic component of telomerase. Transcription factor binding, chromatin status as well as epigenetic modifications at the TERT promoter regulates TERT transcription. Myc is an important transcriptional regulator of TERT that directly controls its expression by promoter binding and associating with other transcription factors. In this review, we discuss the current understanding of the molecular mechanisms behind regulation of TERT transcription by Myc. We also discuss future perspectives in investigating the regulation of Myc at TERT promoter during cancer development.
Highlights
Telomerase is a reverse transcriptase that elongates telomeres (Blackburn and Collins, 2011)
Myc represents an important regulator of telomerase reverse transcriptase (TERT) transcription (Wu et al, 1999; Takahashi et al, 2007; Marion et al, 2009)
We describe how multiple cellular signals impinge on Myc to regulate TERT transcription
Summary
Telomerase is a reverse transcriptase that elongates telomeres (Blackburn and Collins, 2011). It is a ribonucleoprotein composed of a catalytic subunit telomerase reverse transcriptase (TERT), an RNA template Terc and accessory proteins (Cohen et al, 2007; Venteicher et al, 2009). While Terc and other accessory proteins are ubiquitously expressed, TERT is transcriptionally downregulated, thereby limiting telomerase activity in somatic cells (Avilion et al, 1996; Heiss et al, 1998; Holzmann et al, 1998; Parfait et al, 2000; Wang and Zhu, 2004; Wang et al, 2009). Investigating transcriptional regulation of TERT is important for understanding cancer development
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