Matches in SemOpenAlex for { <https://semopenalex.org/work/W1445521649> ?p ?o ?g. }
Showing items 1 to 84 of
84
with 100 items per page.
- W1445521649 endingPage "1255" @default.
- W1445521649 startingPage "1255" @default.
- W1445521649 abstract "Proc Amer Assoc Cancer Res, Volume 47, 20065352 Objectives: In the normal endometrium, progesterone antagonizes the actions of estrogen and inhibits estrogen-induced cellular proliferation. Consequently, progestins have had some therapeutic benefit in the treatment of endometrial cancer. Telomerase activity is dynamic throughout the menstrual cycle and is highest during the proliferative phase under the influence of estrogen and then falls during the secretory phase under the influence of progesterone. Despite this observation, little is known regarding the role of progesterone in the control of telomerase expression. Thus, our goal was to determine progesterone’s role in regulation of telomerase activity in progesterone receptor (PR)-positive endometrial cancer cell lines. Mehods: In our lab, Ishikawa and ECC-1 cells have been previously shown to be estrogen receptor (ER) and PR-positive, and HEC-1B and RL 95-2 cells to be ER and PR-negative. Telomerase activity was assayed using a PCR-based telomeric repeat amplification protocol (TRAP) after cells were exposed to estradiol (E2), medroxyprogesterone acetate (MPA) or both. hTERT mRNA expression was assessed by real-time RT-PCR. To determine whether progesterone regulates transcripton of the hTERT gene, transient expression assays using luciferase reporter plasmids containing varying lengths of the 5’ promoter region of the hTERT gene were performed. Results: Among the PR-positive endometrial cancer cell lines, E2 (10−5 - 10−7 M) increased telomerase activity and hTERT mRNA expression in a dose-dependent manner. In contrast, MPA (10−6 M) inhibited E2 induced telomerase activity in the PR-positive endometrial cancer cell lines by 24 hours. This effect was not seen in the PR-negative endometrial cancer cell lines. hTERT mRNA levels were decreased parallel to suppression of telomerase activity. Luciferase assays demonstrated that exposure to MPA inhibited E2-induced activation of the hTERT promoter which contains two putative estrogen response elements (EREs) but no progesterone response elements (PREs). Conclusions: We provide evidence that progesterone suppresses estrogen-induced hTERT mRNA expression in PR-positive endometrial cancer cell lines. Downregulation of the PR and reactivation of telomerase activity are thought to occur in advanced stages of endometrial cancer; and thus, may be related. Further work focused on the interaction between progesterone, estrogen and telomerase may provide insight into endometrial carcinogenesis as well as the underlying molecular mechanisms of progestins as a targeted therapy for this estrogen-dependent tumor." @default.
- W1445521649 created "2016-06-24" @default.
- W1445521649 creator A5007925500 @default.
- W1445521649 creator A5041232511 @default.
- W1445521649 creator A5063523041 @default.
- W1445521649 creator A5084844090 @default.
- W1445521649 date "2006-04-15" @default.
- W1445521649 modified "2023-10-15" @default.
- W1445521649 title "Progesterone regulation of hTERT transcription in human endometrial cancer cells." @default.
- W1445521649 hasPublicationYear "2006" @default.
- W1445521649 type Work @default.
- W1445521649 sameAs 1445521649 @default.
- W1445521649 citedByCount "0" @default.
- W1445521649 crossrefType "journal-article" @default.
- W1445521649 hasAuthorship W1445521649A5007925500 @default.
- W1445521649 hasAuthorship W1445521649A5041232511 @default.
- W1445521649 hasAuthorship W1445521649A5063523041 @default.
- W1445521649 hasAuthorship W1445521649A5084844090 @default.
- W1445521649 hasConcept C104317684 @default.
- W1445521649 hasConcept C121608353 @default.
- W1445521649 hasConcept C125593758 @default.
- W1445521649 hasConcept C126322002 @default.
- W1445521649 hasConcept C134018914 @default.
- W1445521649 hasConcept C185592680 @default.
- W1445521649 hasConcept C2776306185 @default.
- W1445521649 hasConcept C2777088508 @default.
- W1445521649 hasConcept C2777164284 @default.
- W1445521649 hasConcept C502942594 @default.
- W1445521649 hasConcept C530470458 @default.
- W1445521649 hasConcept C55493867 @default.
- W1445521649 hasConcept C71924100 @default.
- W1445521649 hasConcept C84606932 @default.
- W1445521649 hasConcept C86803240 @default.
- W1445521649 hasConcept C94581717 @default.
- W1445521649 hasConcept C96232424 @default.
- W1445521649 hasConcept C98717036 @default.
- W1445521649 hasConceptScore W1445521649C104317684 @default.
- W1445521649 hasConceptScore W1445521649C121608353 @default.
- W1445521649 hasConceptScore W1445521649C125593758 @default.
- W1445521649 hasConceptScore W1445521649C126322002 @default.
- W1445521649 hasConceptScore W1445521649C134018914 @default.
- W1445521649 hasConceptScore W1445521649C185592680 @default.
- W1445521649 hasConceptScore W1445521649C2776306185 @default.
- W1445521649 hasConceptScore W1445521649C2777088508 @default.
- W1445521649 hasConceptScore W1445521649C2777164284 @default.
- W1445521649 hasConceptScore W1445521649C502942594 @default.
- W1445521649 hasConceptScore W1445521649C530470458 @default.
- W1445521649 hasConceptScore W1445521649C55493867 @default.
- W1445521649 hasConceptScore W1445521649C71924100 @default.
- W1445521649 hasConceptScore W1445521649C84606932 @default.
- W1445521649 hasConceptScore W1445521649C86803240 @default.
- W1445521649 hasConceptScore W1445521649C94581717 @default.
- W1445521649 hasConceptScore W1445521649C96232424 @default.
- W1445521649 hasConceptScore W1445521649C98717036 @default.
- W1445521649 hasLocation W14455216491 @default.
- W1445521649 hasOpenAccess W1445521649 @default.
- W1445521649 hasPrimaryLocation W14455216491 @default.
- W1445521649 hasRelatedWork W1583484284 @default.
- W1445521649 hasRelatedWork W1967387654 @default.
- W1445521649 hasRelatedWork W1968162784 @default.
- W1445521649 hasRelatedWork W1970466057 @default.
- W1445521649 hasRelatedWork W1987819795 @default.
- W1445521649 hasRelatedWork W2011881476 @default.
- W1445521649 hasRelatedWork W2014232493 @default.
- W1445521649 hasRelatedWork W2032248685 @default.
- W1445521649 hasRelatedWork W2033497799 @default.
- W1445521649 hasRelatedWork W2086056180 @default.
- W1445521649 hasRelatedWork W2105083658 @default.
- W1445521649 hasRelatedWork W2134470231 @default.
- W1445521649 hasRelatedWork W2136432553 @default.
- W1445521649 hasRelatedWork W2156773126 @default.
- W1445521649 hasRelatedWork W2347460636 @default.
- W1445521649 hasRelatedWork W2615966397 @default.
- W1445521649 hasRelatedWork W2886590994 @default.
- W1445521649 hasRelatedWork W31847455 @default.
- W1445521649 hasRelatedWork W2358867702 @default.
- W1445521649 hasRelatedWork W2787013832 @default.
- W1445521649 hasVolume "66" @default.
- W1445521649 isParatext "false" @default.
- W1445521649 isRetracted "false" @default.
- W1445521649 magId "1445521649" @default.
- W1445521649 workType "article" @default.