Signalling pathways involved in antitumoral effects of VIP in human renal cell carcinoma A498 cells: VIP induction of p53 expression

被引：5
作者：
Vacas, Eva [1 ]
Munoz-Moreno, Laura [1 ]
Fernandez-Martinez, Ana B. [1 ]
Bajo, Ana M. [1 ]
Sanchez-Chapado, Manuel [2 ,3 ]
Prieto, Juan C. [1 ]
Carmena, Maria J. [1 ]
机构：
[1] Univ Alcala, Unit Biochem & Mol Biol, Dept Syst Biol, Alcala De Henares 28871, Spain
[2] Univ Alcala, Surg Unit, Dept Surg & Med & Social Sci, Alcala De Henares 28871, Spain
[3] Principe Asturias Hosp, Dept Urol, Alcala De Henares 28871, Spain
来源：
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2014年 / 53卷
关键词：
VIP; PI3K; VEGF; p53; Renal cell carcinoma; VASOACTIVE-INTESTINAL-PEPTIDE; CYCLASE-ACTIVATING POLYPEPTIDE; OXIDATIVE STRESS; CANCER; STIMULATION; RECEPTORS; THERAPY; MODELS; TARGET;
D O I：
10.1016/j.biocel.2014.05.036
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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 mu M VIP and/or specific 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 specific p53 inhibitor, cyclin pifithrin-alpha, hydrobromide (CPFT-alpha 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. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码：295 / 301
页数：7
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