Signalling pathways involved in antitumoral effects of VIP in human renal cell carcinoma A498 cells: VIP induction of p53 expression
Authors
Vacas Oliva, Eva; Muñoz Moreno, Laura; Fernández Martínez, Ana Belén; Bajo Chueca, Ana María; Sánchez Chapado, Manuel Vicente; [et al.]Identifiers
Permanent link (URI): http://hdl.handle.net/10017/59408DOI: 10.1016/j.biocel.2014.05.036
ISSN: 13572725
Date
2014-06-04Funders
Ministerio de Ciencia e Innovación
Junta de Comunidades de Castilla-La Mancha
Fundación Mutua Madrileña
Fundación Jesús Serra
Bibliographic citation
The International Journal of Biochemistry & Cell Biology, 2014, v. 53, p. 295-301
Keywords
PI3K
Renal cell carcinoma
VEGF
VIP
p53
Project
info:eu-repo/grantAgreement/MICINN//SAF2007-63794/ES/
info:eu-repo/grantAgreement/JCCM//PII-1%2F09-0061-3802/ES/
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/aceptedVersion
Rights
Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
© Elsevier
Access rights
info:eu-repo/semantics/openAccess
Abstract
Vasoactive intestinal peptide (VIP) decreases cell proliferation through PI3K signalling and prevents tumour progression in clear renal cell carcinoma (RCC). Here we analyzed the signalling pathways that mediate such VIP effects by using human RCC A498 cells. The effects of treatment with 1 mM VIP and/or speci?c protein kinase inhibitors such as H89, Wortmannin and PD98059 were studied by cell adhesion assay, ELISA of VEGF165 and ROS production assays. Semiquantitative RT-PCR and western blot were performed to study p53 expression. VIP increased cell adhesion and ROS production, and decreased VEGF165 secretion through PI3K signalling. Moreover, VIP increased nuclear expression of tumour suppressor p53. VIP effects could be blocked by cell incubation with a speci?c p53 inhibitor, cyclin pi?thrin-a hydrobro- mide (CPFT-?H). In conclusion, this study provides a p53-dependent mechanism by which VIP regulates cell proliferation in RCC development. It supports a potential usefulness of VIP in new therapies of RCC.
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