Enhanced caveolin-1 expression increases migration, anchorage-independent growth and invasion of endometrial adenocarcinoma cells

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dc.contributor.authorDiaz Valdivia, Natalia.
dc.contributor.authorOwen, Gareth Ivor
dc.contributor.authorBravo, Denisse.
dc.contributor.authorHuerta, Hernán.
dc.contributor.authorHenriquez, Soledad.
dc.contributor.authorGabler, Fernando.
dc.contributor.authorVega, Margarita.
dc.contributor.authorRomero, Carmen.
dc.contributor.authorCalderon, Claudia.
dc.contributor.authorLeyton, Lisette.
dc.contributor.authorQuest, Andrew F. G.
dc.date.accessioned2019-10-17T13:39:23Z
dc.date.available2019-10-17T13:39:23Z
dc.date.issued2015
dc.date.updated2019-10-14T18:36:09Z
dc.description.abstractAbstract Background Caveolin-1 (CAV1) has been implicated both in tumor suppression and progression, whereby the specific role appears to be context dependent. Endometrial cancer is one of the most common malignancies of the female genital tract; however, little is known about the role of CAV1 in this disease. Methods Here, we first determined by immunohistochemistry CAV1 protein levels in normal proliferative human endometrium and endometrial tumor samples. Then using two endometrial cancer cell lines (ECC: Ishikawa and Hec-1A) we evaluated mRNA and protein levels of CAV1 by real time qPCR and Western blot analysis, respectively. The role of CAV1 expression in ECC malignancy was further studied by either inducing its expression in endometrial cancer cells with the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (4β-TPA) or decreasing expression using short-hairpin RNA constructs, and then evaluating the effects of these changes on ECC proliferation, transmigration, matrigel invasion, and colony formation in soft agar. Results Immunohistochemical analysis of endometrial epithelia revealed that substantially higher levels of CAV1 were present in endometrial tumors than the normal proliferative epithelium. Also, in Ishikawa and Hec-1A endometrial cancer cells CAV1 expression was readily detectable. Upon treatment with 4β-TPA CAV1 levels increased and coincided with augmented cell transmigration, matrigel invasion, as well as colony formation in soft agar. Reduction of CAV1 expression using short-hairpin RNA constructs ablated these effects in both cell types whether treated or not with 4β-TPA. Alternatively, CAV1 expression appeared not to modulate significantly proliferation of these cells. Conclusion Our study shows that elevated CAV1, observed in patients with endometrial cancer, is linked to enhanced malignancy of endometrial cancer cells, as evidenced by increased migration, invasion and anchorage-independent growth.
dc.fuente.origenBiomed Central
dc.identifier.citationBMC Cancer. 2015 Jun 10;15(1):463
dc.identifier.doi10.1186/s12885-015-1477-5
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/26641
dc.issue.numeroNo.463
dc.language.isoen
dc.nota.accesoContenido completo
dc.pagina.final11
dc.pagina.inicio1
dc.revistaBMC Canceres_ES
dc.rightsacceso abierto
dc.rights.holderDiaz et al.
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.otherEndomerio - Cánceres_ES
dc.subject.otherEndometriosises_ES
dc.subject.otherCaveolina 1es_ES
dc.titleEnhanced caveolin-1 expression increases migration, anchorage-independent growth and invasion of endometrial adenocarcinoma cellses_ES
dc.typeartículo
dc.volumenVol. 15
sipa.codpersvinculados122470
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