Recently, ASF1a has been shown to be up-regulated in certain human malignancies and required for the expression of telomerase reverse transcriptase (TERT), a factor essential for the immortal phenotype of cancer cells; however, its role in oncogenesis remains poorly defined.
The tumorigenesis, development, dedifferentiation and metastasis of ATC are closely associated with the activation of various tyrosine cascades and inactivation of tumor suppressor genes, including B-Raf proto-oncogene, serine/threonine kinase<sup>V600E</sup>, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α,tumor protein 53 mutations and telomerase reverse transcriptase mutation.
Telomerase reverse transcriptase (TERT) has a well-known role in carcinogenesis due to its functions in inducing cell immortality and preventing senescence.
Given these key roles of telomerase and TERT in oncogenesis, great efforts have been made to decipher mechanisms underlying telomerase activation and TERT induction.
By contrast, TERT mutations were not significantly associated with any clinical parameters; therefore, its role in initial tumorigenesis should be further investigated.
It also activates E-box-mediated transcription of various target genes including telomerase reverse transcriptase (TERT) that is involved in cellular immortality and tumorigenesis.
It is established that induction of the telomerase reverse transcriptase gene (<i>TERT</i>) coupled with telomerase activation is essential for cancer development/progression and aberrant <i>TERT</i> promoter methylation of specific 5'-C-phosphate-G-3' (CpGs) has been linked to <i>TERT</i> induction in oncogenesis.
These findings provide insight into the role of <i>TERT</i> in ALM tumorigenesis and reveal preliminary evidence that TERT inhibition represents a potential therapeutic strategy in ALM.
Mutations in the telomerase reverse transcriptase gene promoter (TERTp) are common in glioblastomas (GBMs) and oligodendrogliomas (ODGs), and therefore, have a key role in tumorigenesis and may be of prognostic value.
Transcriptional activation of the human telomerase reverse transcriptase (<i>hTERT</i>) gene, which remains repressed in adult somatic cells, is critical during tumorigenesis.
Telomere length, RTEL1 and TERT expression may serve as potential biomarkers related to silica exposure and may offer insight into the molecular mechanism of silica-induced lung disease and tumorigeneses.
Therefore, we propose that loss of CTCF-dependent imprinting of tumor-promoting genes, such as IGF2 and TERT, results from a defective TGF-β pathway and is responsible at least in part for BWS-associated tumorigenesis as well as sporadic human cancers that are frequently associated with SPTBN1 and SMAD3 mutations.
Our results suggest that TERT reactivation through promoter mutation either alone or in association with the HPV oncogenes (E6 and E7) could play an important role in the carcinogenesis of cervical and oral cancers.
We found differences in the expression between alleles and in the regulation of several genes involved in cancer, such as TP53, KIT, CDH1, CLH, and TERT, which may result in changes in regulatory networks related to tumorigenesis.
Telomerase reverse transcriptase (TERT) expression is a hallmark in tumorigenesis and upregulated due to mutations and methylation of the human (h)TERT promoter.
Based on these data, we conclude that reactivation of TERT, a direct transcriptional MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis.