Vasoactive intestinal peptide increases vascular endothelial growth factor expression and neuroendocrine differentiation in human prostate cancer LNCaP cells

Collado, Beatriz; Gutiérrez‐Cañas, Irene; Rodríguez-Henche, Nieves; Prieto, Juan Carlos; Carmena, Marı́a J.

doi:10.1016/j.regpep.2004.01.013

Cited by 43 publications

(23 citation statements)

References 32 publications

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“…The effect was mediated by the VPAC 1 -R, because the agonists of this R but not of VPAC 2 -R, mimicked VIP and PACAP action. Moreover, it occurred via the activation of PKA-, PI3K-, and ERK1/2-dependent pathways, because it was suppressed by H89, wortmanin, and PD98059 exposure (Collado et al, 2004(Collado et al, , 2005. Hypoxia up-regulated VIP expression in LNCaP cells, and VIP raised the expression of PAC 1 -Rs and VPAC 1 -Rs and decreased that of VPAC 2 -Rs.…”

Section: H Vasoactive Intestinal Peptide and Pituitary Adenylate Cycmentioning

confidence: 99%

Nonclassic Endogenous Novel Regulators of Angiogenesis

Ribatti

Conconi²,

Nussdorfer³

2007

Pharmacol Rev

162

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Angiogenesis, the process through which new blood vessels arise from preexisting ones, is regulated by several "classic" factors, among which the most studied are vascular endothelial growth factor ( VEGF) and fibroblast growth factor-2 (FGF- 2). In recent years, investigations showed that, in addition to the classic factors, numerous endogenous peptides play a relevant regulatory role in angiogenesis. Such regulatory peptides, each of which exerts well-known specific biological activities, are present, along with their receptors, in the blood vessels and may take part in the control of the "angiogenic switch." An in vivo and in vitro pro-angiogenic effect has been demonstrated for erythropoietin, angiotensin II (ANG- II), endothelins (ETs), adrenomedullin (AM), proadrenomedullin N-terminal 20 peptide (PAMP), urotensin-II, leptin, adiponectin, resistin, neuropeptide- Y, vasoactive intestinal peptide ( VIP), pituitary adenylate cyclase- activating polypeptide ( PACAP), and substance P. There is evidence that the angiogenic action of some of these peptides is at least partly mediated by their stimulating effect on VEGF ( ANG- II, ETs, PAMP, resistin, VIP and PACAP) and/ or FGF-2 systems ( PAMP and leptin). AM raises the expression of VEGF in endothelial cells, but VEGF blockade does not affect the proangiogenic action of AM. Other endogenous peptides have been reported to exert an in vivo and in vitro antiangiogenic action. These include somatostatin and natriuretic peptides, which suppress the VEGF system, and ghrelin, that antagonizes FGF- 2 effects. Investigations on "nonclassic" regulators of angiogenesis could open new perspectives in the therapy of diseases coupled to dysregulation of angiogenesis

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Section: H Vasoactive Intestinal Peptide and Pituitary Adenylate Cycmentioning

confidence: 99%

Nonclassic Endogenous Novel Regulators of Angiogenesis

Ribatti

Conconi²,

Nussdorfer³

2007

Pharmacol Rev

162

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“…8 To date, several signals have been reported to induce NE transdifferentiation in cultured PCa cells, including androgen withdrawal, 8 cAMP, interleukin (IL)-6, 9 antioxidants 10,11 or vasoactive intestinal peptide (VIP). 12 These studies have brought some light about the molecular mechanisms involved in this intriguing process and yet many aspects remain elusive.…”

mentioning

confidence: 99%

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

Quiros

Sáinz

Hevia

et al. 2009

Intl Journal of Cancer

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Despite improvements in diagnosis of advanced prostate cancer (PCa), treatment is not efficient and 5-year survival is still low. Initially, the less abundant of cell types, neuroendocrine cells (NE), are involved in regulatory process but their physiological role is not fully understood. Among others, an increase in NE cells along with tumor progression has been commonly reported but their role in tumorigenesis or the molecular mechanisms of transdifferentiation is still a matter of debate. We have used human PCa cells (LNCaP) induced to differentiate to NE cells with several stimuli: androgen withdrawal, cyclic AMP or treatment with the antioxidant pineal hormone melatonin. PCa patients' specimens were also analyzed by western blotting and by immunocytochemistry. NE-like LNCaP cells express high levels of mitochondrial superoxide dismutase (MnSOD/SOD2) in addition to NE markers. MnSOD upregulation is mediated by NFjB transcription factor, mainly through p65 translocation into the nuclei. More importantly, overexpression of MnSOD induces the rise of NE-markers in LNCaP cells, showing that MnSOD upregulation might be instrumental for NE differentiation in PCa cells. Furthermore, MnSOD is highly expressed in advanced tumors of patients' when compared with control, nonpathological samples or with low-grade tumors, along with the presence of synaptophysin, a common NE marker. Also, fluorescence immunohistochemical analysis revealed that MnSOD colocalizes with NE markers in most of NE cells observed in PCa specimens. The present findings indicate that MnSOD is essential for NE transdifferentiation and mediates in part the differentiation process, which appears also to be critical in vivo. ' 2009 UICC

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“…NE differentiation was later shown to be induced in LNCaP cells by the depletion of steroid [26,27], or by the addition of interleukins (IL) 1, 2 or 6 [28,29] to the culture medium. Various neuropeptides, such as Vasoactive Intestinal Peptide (VIP) [30][31][32] …”

Section: Cell Models For Ne Differentiationmentioning

confidence: 99%

“…In LNCaP cells, it has been shown that VIP, a neuropeptide inducing the expression of NE markers, such as NSE and CgA [30,32], also rapidly increases cytosolic calcium levels, c-Fos proto-oncogene and VEGF mRNA expression. This is associated with VEGF secretion and neurite lengthening.…”

Section: Signalling Pathways and Role Of Calciummentioning

confidence: 99%

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

Warnier¹,

Gackière²,

Roudbaraki³

et al. 2017

J Cell Signal

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Neuroendocrine cells release their secretion into the extracellular environment through calcium-dependent signalling pathways. These cells share common morphological and molecular features such as the expression of specific biomarkers, neurite outgrowth and dense core secretory granules. In order to elucidate the signalling pathways leading from undifferentiated to differentiated neuroendocrine cells, the role of voltage-dependent calcium channels, central actors in the excitation-secretion coupling, has been comprehensively investigated. T-type calcium channels appear to belong to the most important ion channel family involved in the neuroendocrine differentiation process. They could also participate in the development of neuroendocrine tumours.

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Vasoactive intestinal peptide increases vascular endothelial growth factor expression and neuroendocrine differentiation in human prostate cancer LNCaP cells

Cited by 43 publications

References 32 publications

Nonclassic Endogenous Novel Regulators of Angiogenesis

Nonclassic Endogenous Novel Regulators of Angiogenesis

Upregulation of manganese superoxide dismutase (SOD2) is a common pathway for neuroendocrine differentiation in prostate cancer cells

Expression and Role of T-type Calcium Channels during Neuroendocrine Differentiation

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