Expression of vasoactive intestinal peptide and functional VIP receptors in human prostate cancer: Antagonistic action of a growth-hormone-releasing hormone analog

Collado, Beatriz; Carmena, Marı́a J.; Sánchez‐Chapado, Manuel; Ruíz-Villaespesa, Antonio; Bajo, Ana M.; Fernández‐Martínez, Ana B.; Varga, József; Prieto, Juan Carlos

doi:10.3892/ijo.26.6.1629

Cited by 18 publications

(13 citation statements)

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“…It has been shown that small G-protein Rap1 plays a key role in hormonal activation of ERKs via G s -coupled receptors in a number of systems, including those involving isoproterenol in S49 mouse lymphoma cells (Wan and Huang, 1998), thyroid-stimulating hormone in FRTL-5 rat thyroid cells (Iacovelli et al, 2001), and VIP in pituitary cells (Fernandez et al, 2005). However, the role of PKA in Rap1 activation remains controversial and may be cell-dependent, as shown in those studies.…”

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confidence: 92%

“…Previous studies have shown that MAPKs, particularly ERK1/2, are involved in androgen-independent AR activation in prostate cancer cells (Cao et al, 2006). It is interesting that VIP activated ERK1/2 in pituitary cells (Fernandez et al, 2005) and potentiated the ability of EGF, interleukin 6, and serum to activate MAPK in LNCaP cells (Chen et al, 1999). Thus, we examined ERK activity in LNCaP cells after VIP treatment through the measurement of ERK-activated, Elk-1-dependent expression of a luciferase reporter gene (Cao et al, 2006).…”

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confidence: 99%

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Vasoactive Intestinal Peptide Transactivates the Androgen Receptor through a Protein Kinase A-Dependent Extracellular Signal-Regulated Kinase Pathway in Prostate Cancer LNCaP Cells

Xie

Wolff

Lin³

et al. 2007

Mol Pharmacol

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Acquisition of androgen independence by prostate cancer is the key problem of prostate cancer progression. Vasoactive intestinal peptide (VIP), a neuropeptide, may act as a survival factor for prostate cancer cells under androgen deprivation. However, the molecular mechanisms by which VIP promotes the androgenindependent growth of androgen-sensitive prostate cancer cells have not been addressed. We therefore investigated the biological effect and signal pathway of VIP in LNCaP cells, a prostate cancer cell line that requires androgens for growth. We showed that low nanomolar concentrations of VIP, acting through G s -protein-coupled VIP receptors, can induce LNCaP cell growth in the absence of androgen. Blockade of androgen-receptor (AR) in these cells by AR antagonist bicalutamide or by anti-AR small interfering RNA, inhibited the proliferative effect of VIP. In addition, VIP stimulated androgen-independent activation of AR with an EC 50 of 3.0 Ϯ 0.8 nM. We then investigated VIP-stimulated signaling events that may interact with the AR pathway in prostate cancer cells. VIP regulation of AR activation, mediated by VIP receptors, was protein kinase A (PKA)-dependent, and extracellular signal-regulated kinase 1/2 (ERK1/2) activation contributes to VIP-mediated AR activation. Furthermore, PKA-dependent Rap1 activation is required for both ERK1/2 activation and androgen-independent AR activation in LNCaP cells upon VIP stimulation. Finally, we showed that VIP-induced AR activation was also present in prostate cancer CWR22Rv1 and PC3 cells transfected with the wild-type AR. Altogether, we demonstrate that VIP acting through its G s -proteincoupled receptors can cause androgen-independent transactivation of AR through a PKA/Rap1/ERK1/2 pathway, thus promoting androgen-independent proliferation of androgen-sensitive prostate cancer cells.Prostate cancer is the most commonly diagnosed noncutaneous cancer in American men and the second leading cause (after lung) of cancer mortality. In its early stages, prostate cancer cell growth is dependent on androgens and their androgen receptor (AR), a member of the nuclear receptor superfamily (Heinlein and Chang, 2004). Thus, androgen-deprivation therapies that block AR activation cause repression of prostate tumors. Unfortunately, the majority of prostate cancers eventually transit from being androgen-dependent to androgen-independent (hormone refractory), making androgen-deprivation therapies ineffective (Feldman and Feldman, 2001).The precise mechanisms underlying this conversion of

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Section: Downloaded Frommentioning

confidence: 92%

Section: Downloaded Frommentioning

confidence: 99%

Vasoactive Intestinal Peptide Transactivates the Androgen Receptor through a Protein Kinase A-Dependent Extracellular Signal-Regulated Kinase Pathway in Prostate Cancer LNCaP Cells

Xie

Wolff

Lin³

et al. 2007

Mol Pharmacol

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“…Neoplastic cells from breast, lung, and prostate, as well as pancreatic, colonic, and hepatocellular carcinoma, often express type II PACAP/VIP binding sites (Reubi, 1995;Moody et al, 1998;Reubi et al, 1999a,b;Busto et al, 1999Busto et al, , 2003Germano et al, 2004;Schulz et al, 2004;Collado et al, 2005;García-Ferná ndez et al, 2005;Mammi et al, 2006;Moretti et al, 2006). The presence of type II recognition sites also occurs in human pituitary adenoma (Robberecht et al, 1993;Oka et al, 1998) and brain glioma Vertongen et al, 1995a;Sokolowska and Nowak, 2006).…”

Section: G Pituitary Adenylate Cyclase-activating Polypeptide Receptmentioning

confidence: 99%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…GPCR agonists, such as endothelin-1, bombesin, calcitonin, and vasoactive intestinal polypeptide (VIP), have been shown to support androgen-independent growth of prostate cancer cells (26,27). Elevated expression of VIP and VIP receptors has been found in prostate carcinoma, and antagonists of VIP inhibit the growth of prostate cancer xenografts (28,29). VIP is secreted by autonomous nerves in the prostate gland and also can be produced by prostate cancer cells (27, 30 -32).…”

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confidence: 99%

Diverse Antiapoptotic Signaling Pathways Activated by Vasoactive Intestinal Polypeptide, Epidermal Growth Factor, and Phosphatidylinositol 3-Kinase in Prostate Cancer Cells Converge on BAD

Sastry

Smith

Karpova

et al. 2006

Journal of Biological Chemistry

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It has been demonstrated that vasoactive intestinal polypeptide, epidermal growth factor, and chronic activation of phosphatidylinositol 3-kinase can protect prostate cancer cells from apoptosis; however, the signaling pathways that they use and molecules that they target are unknown. We report that vasoactive intestinal polypeptide, epidermal growth factor, and phosphatidylinositol 3-kinase activate independent signaling pathways that phosphorylate the proapoptotic protein BAD. Vasoactive intestinal polypeptide operated via protein kinase A, epidermal growth factor required Ras activity, and effects of phosphatidylinositol 3-kinase were predominantly mediated by Akt. BAD phosphorylation was critical for the antiapoptotic effects of each signaling pathway. None of these survival signals was able to rescue cells that express BAD with mutations in phosphorylation sites, whereas knockdown of BAD expression with small hairpin RNA rendered cells insensitive to apoptosis. Taken together, these results identify BAD as a convergence point of several antiapoptotic signaling pathways in prostate cells.

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Expression of vasoactive intestinal peptide and functional VIP receptors in human prostate cancer: Antagonistic action of a growth-hormone-releasing hormone analog

Cited by 18 publications

References 0 publications

Vasoactive Intestinal Peptide Transactivates the Androgen Receptor through a Protein Kinase A-Dependent Extracellular Signal-Regulated Kinase Pathway in Prostate Cancer LNCaP Cells

Vasoactive Intestinal Peptide Transactivates the Androgen Receptor through a Protein Kinase A-Dependent Extracellular Signal-Regulated Kinase Pathway in Prostate Cancer LNCaP Cells

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Diverse Antiapoptotic Signaling Pathways Activated by Vasoactive Intestinal Polypeptide, Epidermal Growth Factor, and Phosphatidylinositol 3-Kinase in Prostate Cancer Cells Converge on BAD

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