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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: Mechanisms of human telomerase reverse transcriptase (hTERT) regulation: clinical impacts in cancer

Fig. 2

Mechanisms of hTERT regulation in cancer. Transcription factors and their binding sites, as well the positions of both hTERT promoter mutations, C228T and C250T, the hypermethylated region upstream to TSS (THOR) and TERT-miRNAs are shown. The cancer-specific mutations within the core promoter, at -124 and -146bp positions generate ETS binding motifs, leading to GABP transcription factor recruitment and consequently hTERT transcription. Binding of transcriptional activators (c-Myc) and repressors (WT1 and CTCF) to the hTERT promoter may be controlled by DNA methylation, in which methylated CpGs prevent their binding to the target sites, leading to hTERT activation (THOR region). MiRNAs targeting the 3’UTR promotes translation repression of hTERT. Black dots represent methylated CpG sites. ETS: E-twenty-six; TSS: transcription start site; ATG: start codon

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