Abstract
Telomeres at the termini of human chromosomes are shortened with each round of cell division due to the “end replication problem” as well as oxidative stress. During carcinogenesis, cells acquire or retain mechanisms to maintain telomeres to avoid initiation of cellular senescence or apoptosis and halting cell division by critically short telomeres. The unique reverse transcriptase enzyme complex, telomerase, catalyzes the maintenance of telomeres but most human somatic cells do not have sufficient telomerase activity to prevent telomere shortening. Tissues with high and prolonged replicative potential demonstrate adequate cellular telomerase activity to prevent telomere erosion, and high telomerase activity appears to be a critical feature of most (80–90%) epithelial cancers, including endometrial cancer. Endometrial cancers regress in response to progesterone which is frequently used to treat advanced endometrial cancer. Endometrial telomerase is inhibited by progestogens and deciphering telomere and telomerase biology in endometrial cancer is therefore important, as targeting telomerase (a downstream target of progestogens) in endometrial cancer may provide novel and more effective therapeutic avenues. This review aims to examine the available evidence for the role and importance of telomere and telomerase biology in endometrial cancer.
Highlights
Telomeres are specialized structures that are found at the ends of linear chromosomes, containing a tandemly repeated specific deoxyribonucleic acids (DNA) sequence and associated protective proteins
In recurrent reproductive failure samples, the immunostaining for telomerase was significantly high in various endometrial cellular compartments and this indicates that there are specific alterations occur in the regulation of endometrial cell fate are associated with recurrent reproductive failure various types Either weak or absent telomerase immunoreactivity was observed in the endometria of fertile healthy women throughout the luteal phase
The mean TL were significantly longer in endometria of women with endometriosis during the implantation window This study suggested that aberrant expression of telomerase in endometrium alters the cell fate and enhances the cellular proliferation and that leads to the occurrence of endometriosis In endometrial polyp tissue, the level of telomerase was decreased in comparison with normal endometrial tissue
Summary
Telomeres are specialized structures that are found at the ends of linear chromosomes, containing a tandemly repeated specific DNA sequence and associated protective proteins. The protective function of telomeres in preventing the loss of genomic DNA in proliferating cells is well-established [1,2,3]. Oxidative stress is an important additional cause for telomere shortening [6, 7]. Telomerase is a unique reverse transcriptase enzyme [8] that is able to add repetitive telomeric sequences de novo onto telomeric ends [9] that are continually lost during DNA replication due to oxidative stress and the “end replication problem” in mitotic cells. Most human somatic cells do not have significant levels of telomerase activity whereas cells, such as embryonic stem cells and most cancer cells exhibit high telomerase activity while adult tissue stem cells are potentially able to up-regulate telomerase upon activation [10,11,12]
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