Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/65547
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dc.contributor.authorGomez-Lomeli, P.
dc.contributor.authorBravo-Cuellar, A.
dc.contributor.authorHernandez-Flores, G.
dc.contributor.authorJave-Suarez, L.F.
dc.contributor.authorAguilar-Lemarroy, A.
dc.contributor.authorLerma-Diaz, J.M.
dc.contributor.authorDominguez-Rodriguez, J.R.
dc.contributor.authorSanchez-Reyes, K.
dc.contributor.authorOrtiz-Lazareno, P.C.
dc.date.accessioned2015-11-19T18:50:28Z-
dc.date.available2015-11-19T18:50:28Z-
dc.date.issued2014
dc.identifier.urihttp://hdl.handle.net/20.500.12104/65547-
dc.description.abstractBackground: Natural killer (NK) cells eliminate virus-infected and tumor cells through the release of perforins and granzymes; they also produce Interferon gamma (IFN-γ) and Tumor necrosis factor alpha (TNF-α), which induce apoptosis in target cells. Many tumors express Heme oxygenase 1 (HO-1), and this expression has been associated with avoiding immunosuppression and apoptosis. In this work, HO-1+ Cervical cancer cell (CCC) lines were pre-treated with HO-1 inhibitor and we assessed whether this inhibition enhanced the sensitivity of CCC to NK cell activity.Methods: We assessed the expression of HO-1 in HeLa, SiHa, and C-33A CCC by Flow cytometry (FC). CCC were pre-treated with SnPP or ZnPP HO-1 inhibitors. After that, NK-92 cells were co-cultured with HeLa, SiHa, and C-33A CCC pre-treated or not with HO-1 inhibitors, and the expression of IFN-γ, TNF-α, CD107a, Granzyme B, NKp44, NKp46, NKp30, and NKG2D was evaluated by FC. Results: CCC lines HeLa, SiHa, and C-33A expressed HO-1. Inhibition of HO-1 in these cells increased the expression of IFN-γ and TNF-α in CD107a + NK-92 cells. We observed a reduction in the expression of NKG2D, NKp46, and NKp30 in NK cells co-cultured with HeLa and SiHa cells, and when HeLa and SiHa cells were pre-treated with the HO-1 inhibitors, the expression of NKG2D and NKp30 in NK cells was restored. We observed a similar effect in NK cells co-cultured with C-33A cells in NKp30 expression.Conclusion: Inhibition of HO-1 in CCC induces an increase in IFN-γ and TNF-α production in CD107a + NK-92 cells and restores NKG2D, NKp46 and NKp30 downmodulation in NK cells. © 2014 Gómez-Lomeli et al.; licensee BioMed Central Ltd.
dc.titleIncrease of IFN-γ and TNF-α production in CD107a + NK-92 cells co-cultured with cervical cancer cell lines pre-treated with the HO-1 inhibitor
dc.typeArticle
dc.identifier.doi10.1186/s12935-014-0100-1
dc.relation.ispartofjournalCancer Cell International
dc.relation.ispartofvolume14
dc.relation.ispartofissue1
dc.relation.ispartofpage100
dc.subject.keywordCervical cancer cells; Heme oxygenase 1; IFN-γ; NK cells; NKG2D; NKp30; TNF-α
dc.contributor.affiliationGómez-Lomelí, P., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico, Programa de Doctorado en Ciencias Biomédicas Orientación Inmunología, Centro Universitario de Ciencias de la Salud (CUCS)UdeG, Guadalajara, Jalisco, Mexico; Bravo-Cuellar, A., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico, Departamento de Ciencias de la Salud, Centro Universitario de los Altos, Universidad de Guadalajara (UdeG), Tepatitlán de MorelosJalisco, Mexico; Hernández-Flores, G., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico; Jave-Suárez, L.F., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico; Aguilar-Lemarroy, A., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico; Lerma-Díaz, J.M., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico, Departamento de Ciencias de la Salud, Centro Universitario de los Altos, Universidad de Guadalajara (UdeG), Tepatitlán de MorelosJalisco, Mexico; Domínguez-Rodríguez, J.R., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico, Departamento de Farmacobiología, Centro Universitario de Ciencias Exactas e IngenieríaUdeG, Guadalajara, Jalisco, Mexico; Sánchez-Reyes, K., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico, Programa de Doctorado en Ciencias Biomédicas Orientación Inmunología, Centro Universitario de Ciencias de la Salud (CUCS)UdeG, Guadalajara, Jalisco, Mexico; Ortiz-Lazareno, P.C., División de Inmunología, Centro de Investigación Biomédica de Occidente (CIBO), Instituto Mexicano del Seguro Social (IMSS), Sierra Mojada 800, Col. IndependenciaGuadalajara Jalisco, Mexico
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