Modulation of the expression of the VIP receptor by serum factors on the human melanoma cell line IGR39

Bellan, Catherine; Fabre, Christine; Secchi, J.; Marvaldi, Jacques; Pichon, Jacques; Luis, José

doi:10.1016/s0014-4827(05)80068-0

Cited by 6 publications

(3 citation statements)

References 29 publications

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“…Thus, the apparent up‐regulation of VIP receptors in serum‐starved keratinocytes, may indicate that VIP functions as a survival factor for these cells. Like our results, serum deprivation has been shown before to modulate VIP binding sites in melanoma cells [24]. Since VPAC 2 R expression in starved HaCaT did not show a parallel change, the suggested over‐expression of VPAC 1 R receptor induced by serum starvation is a specific rather than a generalized event.…”

Section: Discussionsupporting

confidence: 83%

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes

Granoth¹,

Fridkin²,

Gozes³

2000

FEBS Letters

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Vasoactive intestinal polypeptide (VIP) exhibits effects on cell proliferation. Here, VIP, as well as the related peptide, pituitary adenylate cyclase activating peptide (PACAP), promoted human keratinocyte division. Stearyl-Nle 17 -VIP (SNV) was identified as a superior mitogen for the keratinocytic cell line, HaCaT, both in potency (fM^nM concentrations) and efficacy. Reverse transcription-polymerase chain reaction detected in keratinocytes only PACAP mRNA and the relevant type 1 (VPAC 1 R) and type 2 (VPAC 2 R) receptors, while VIP and the third receptor (PAC 1 ) transcripts were absent. Upon serum deprivation of HaCaT, the VPAC 1 R mRNA was apparently increased, while the VPAC 2 R transcript remained constant. Incubation of HaCaT with VIP or SNV increased nitric oxide and cGMP formation. In contrast to VIP, SNV did not augment cAMP. Thus, the paracrine VIP, and autocrine PACAP, related pathways leading to keratinocyte proliferation may involve VPAC 1 R/VPAC 2 R and nitric oxide/cGMP production. ß

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Section: Discussionsupporting

confidence: 83%

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes

Granoth¹,

Fridkin²,

Gozes³

2000

FEBS Letters

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“…Bellan et al showed that in a human melanoma cell line (IGR39), VIP binding is inversely correlated with the serum concentration in the culture me‐ dium 37. This effect may be mediated by increases in VPAC1 receptor in starved cells 29.…”

Section: Discussionmentioning

confidence: 99%

A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines

Gelber

Granoth

Fridkin

et al. 2001

Cancer

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BACKGROUND Vasoactive intestinal peptide (VIP) is one of several small neuropeptides that affect cancer growth. A lipophilic VIP analog, stearyl‐Nle17‐neuroten‐ sin6‐11VIP7‐28 (SNH) that inhibited lung carcinoma growth has been described previously. The experiments performed were clonogenic assays in vitro and tumor xenografts in nude mice in vivo. These studies were now extended to colon carcinoma and to combination therapy with chemotherapeutic agents. METHODS Assays were performed with cell lines, and tumor proliferation was assessed using the (3‐[4,5‐dimethylthiazol‐2‐yl‐5]‐[3‐carboxymethoxyphenyl]‐2‐[4‐sulfophenyl]‐2H tetrazolium) (MTS) colorimetric assay for mitochondrial function of living cells. RESULTS The lipophilic analog (SNH) enhanced the antiproliferative activity of diverse chemotherapeutic agents: doxorubicine (antibiotic); vinorelbine (vinca alkaloid, antimicrotubule formation); paclitaxel (antimicrotubule agent); gemcitabine (antimetabolite); irinotecan (topoisomerase I inhibitor); and cisplatin (platinum compound acting as an alkylating agent). In all cases, the antiproliferative effect of SNH and the chemotheraputic agent was at least additive and for some combinations and concentrations even synergistic. For example, 2 μM of the antagonist that produced a 15–20% growth inhibition in the nonsmall cell lung carcinoma cell line reduced the IC50 by 2–4‐fold for most of the chemotherapeutic agents tested. Higher analog concentrations were even more efficacious. Similar results were obtained with colon carcinoma cell lines. CONCLUSIONS Chemotherapeutic treatment of advanced solid tumors, such as nonsmall cell lung carcinoma, colon carcinoma, or prostate carcinoma, achieves a response rate of between 10% and 30% with significant toxicity. Combination therapy with the lipophilic VIP analog SNH and the preferred chemotherapeutic agent may greatly enhance the response rate, and by permitting a dose reduction, should significantly reduce side effects. Cancer 2001;92:2172–80. © 2001 American Cancer Society.

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“…This observation may indicate that the expression of this antigen is not synchronised in all the cells or it can be interpreted as a consequence of the particular geometry of the culture system that might prevent access of the antibody to the antigen. Another possibility would be to assume that, in some cells of HSVEP cultures, the expression of VIP receptors is repressed by some medium factors, as shown in the human melanoma cell line IGR39 (Bellan et al 1992). Another tempting explanation for the patchy pattern of immunoreaction would be that HSVEP heterogeneously express more than one subclass of VIP receptor.…”

Section: Vip Receptor/binding Site Retention In Hsvepmentioning

confidence: 99%

Vasoactive intestinal peptide stimulates apical secretion in hamster seminal vesicle epithelial cells in culture

Rodrigues

Cachaço

Gulbenkian

et al. 1999

Cell and Tissue Research

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In this study, we investigated the presence of vasoactive intestinal peptide (VIP) receptors in the epithelial cells of the hamster seminal vesicle, by using cell clusters isolated from the gland and cultivated in a serum-free bicameral culture system. An immunocytochemical approach and autoradiographic and biochemical binding experiments with 125I-VIP as radioligand were performed. The effect of this neuropeptide on cultured cell proliferation and protein secretory activity was also analysed. The release of trichloroacetic-acid-precipitable radioactive material by epithelial cells to the apical and basal compartments of the bi-chamber was estimated in absolute and relative terms. The results of this work indicate that: (1) VIP receptors are present in the membranes of clusters of epithelial cells from seminal vesicles and are further maintained in cultured cells; (2) VIP does not exert any mitogenic effect in these cells; (3) VIP affects the directionality of secretion, favouring the absolute and relative amounts of protein released to the apical compartment of the bi-chamber. The expression of VIP receptors in the epithelial cells of the hamster seminal vesicle and the direct secretagogue-like activity of this neuropeptide in these cells might be affected by other factors, namely, androgens.

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Modulation of the expression of the VIP receptor by serum factors on the human melanoma cell line IGR39

Cited by 6 publications

References 29 publications

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes

A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines

Vasoactive intestinal peptide stimulates apical secretion in hamster seminal vesicle epithelial cells in culture

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Modulation of the expression of the VIP receptor by serum factors on the human melanoma cell line IGR39

Cited by 6 publications

References 29 publications

VIP and the potent analog, stearyl‐Nle17‐VIP, induce proliferation of keratinocytes

VIP and the potent analog, stearyl‐Nle17‐VIP, induce proliferation of keratinocytes

A lipophilic vasoactive intestinal peptide analog enhances the antiproliferative effect of chemotherapeutic agents on cancer cell lines

Vasoactive intestinal peptide stimulates apical secretion in hamster seminal vesicle epithelial cells in culture

Contact Info

Product

Resources

About

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes

VIP and the potent analog, stearyl‐Nle¹⁷‐VIP, induce proliferation of keratinocytes