The oestrogen metabolite 2-methoxyoestradiol alone or in combination with tumour necrosis factor-related apoptosis-inducing ligand mediates apoptosis in cancerous but not healthy cells of the human endometrium

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dc.contributor.authorKato, Sumie
dc.contributor.authorSadarangani, Anil
dc.contributor.authorLange, Soledad
dc.contributor.authorVillalon, Manuel
dc.contributor.authorBranes, Jorge
dc.contributor.authorBrosens, Jan J.
dc.contributor.authorOwen, Gareth I.
dc.contributor.authorCuello, Mauricio
dc.date.accessioned2024-01-10T14:22:03Z
dc.date.available2024-01-10T14:22:03Z
dc.date.issued2007
dc.description.abstractCancers of the reproductive tract account for 12% of all malignancies in women. As previous studies have shown that oestrogen metabolites can cause apoptosis, we characterised the effect of oestrogen and oestrogen metabolites on non-cancerous and cancerous human endometrial cells. Herein, we demonstrate that 2-methoxyoestradiol (2ME), but not 17 beta-oestradiol, induces apoptosis in cancer cell lines and primary cultured tumours; of endometrial origin. In contrast, 2ME had no effect on cell viability of corresponding normal tissue. This ability of 2ME to induce apoptosis does not require oestrogen receptor activation, but is associated with increased entry into the G2/M phases of the cell cycle and the activation of both the intrinsic and the extrinsic apoptotic pathways. The selective behaviour of 2ME on cancerous as opposed to normal tissue may be due to a reduction in 17 beta -hydroxysteroid dehydrogenase type 11 levels in cancer cells and to a differential down-regulation of superoxide dismutase. Furthermore, we demonstrate that pre-treatment with 2ME enhances the sensitivity of reproductive tract cancer cells to the apoptotic drug tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), without the loss in cell viability to normal cells incurred by currently chemotherapeutic drugs. In conclusion, 2ME, alone or in combination with TRAIL, may be an effective treatment for cancers of uterine origin with minimal toxicity to corresponding healthy female reproductive tissue.
dc.description.funderWellcome Trust
dc.format.extent18 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1677/ERC-07-0008
dc.identifier.eissn1479-6821
dc.identifier.issn1351-0088
dc.identifier.pubmedidMEDLINE:17639050
dc.identifier.urihttps://doi.org/10.1677/ERC-07-0008
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79849
dc.identifier.wosidWOS:000248720300015
dc.information.autorucMedicina;Branes J;S/I;76860
dc.information.autorucMedicina;Cuello M;S/I;80064
dc.information.autorucMedicina;Kato S;S/I;82640
dc.information.autorucCiencias Biológicas;Owen G;S/I;1000459
dc.information.autorucCiencias Biológicas;Villalón M;S/I;99264
dc.issue.numero2
dc.language.isoen
dc.nota.accesoSin adjunto
dc.pagina.final368
dc.pagina.inicio351
dc.publisherBIOSCIENTIFICA LTD
dc.revistaENDOCRINE-RELATED CANCER
dc.rightsregistro bibliográfico
dc.subjectPROSTATE-CANCER
dc.subjectCATECHOL ESTROGENS
dc.subjectCYCLE ARREST
dc.subject2-METHOXYESTRADIOL
dc.subjectBREAST
dc.subjectEXPRESSION
dc.subjectCARCINOMA
dc.subjectLINES
dc.subjectESTRADIOL
dc.subjectALPHA
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleThe oestrogen metabolite 2-methoxyoestradiol alone or in combination with tumour necrosis factor-related apoptosis-inducing ligand mediates apoptosis in cancerous but not healthy cells of the human endometrium
dc.typeartículo
dc.volumen14
sipa.codpersvinculados76860
sipa.codpersvinculados80064
sipa.codpersvinculados82640
sipa.codpersvinculados1000459
sipa.codpersvinculados99264
sipa.indexWOS
sipa.trazabilidadCarga SIPA;09-01-2024
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