Abstract
Objective: Given that prolonged exposure to estrogen and increased telomerase activity are associated with endometrial carcinogenesis, our objective was to evaluate the interaction between the MAPK pathway and estrogen induction of telomerase activity in endometrial cancer cells.
Highlights
Endometrial cancer is the most most common malignancy in women in the United States [1]
We have previously shown that E2 induces telomerase activity and hTERT mRNA expression in estrogen receptor (ER)-positive endometrial cancer cell lines, potentially through binding of complexed estrogen with estrogen receptor-a (ERa) to estrogen response elements (EREs) found within the hTERT promoter
We wanted to elicit the underlying molecular mechanism involved in regulating telomerase activity and hTERT mRNA expression induced by E2 in the ERa-positive Ishikawa cell line
Summary
Endometrial cancer is the most most common malignancy in women in the United States [1]. Human telomeres inevitably undergo progressive shortening in normal somatic cells through the replication-dependent sequence loss at terminal ends of the DNA. Telomerase is a ribonucleoprotein reverse transcriptase that synthesizes telomeric DNA into chromosomal ends. This enzyme recognizes the G-rich strand of an existing telomere repeat sequence and synthesizes a new copy of the repeat sequence in the absence of a complementary DNA strand, with a segment of its internal RNA component serving as a template [3,4]. The expression of hTERT is observed at high levels in telomerase-positive cancer cells but not in telomerase-negative cells, and is considered the rate-limiting determinant of telomerase activity [7,8]
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