Peptide Receptors in Intestinal Epithelium

Laburthe, Marc; Amiranoff, B.

doi:10.1002/cphy.cp060211

Cited by 12 publications

(6 citation statements)

References 333 publications

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“…An early observation suggesting that colon cancers could be responsive to their neurohormonal environment was that human colon cancer cells, like normal colonocytes, express receptors for vasoactive intestinal peptide (VIP), a neuropeptide very abundant in the colon (Laburthe et al, 1978). Consistent with this, various short‐term and long‐term effects of VIP on the metabolism and transport properties of colon cancer cell lines in culture have been reported (Laburthe et al, 1987; Laburthe and Amiranoff, 1989). Receptors or biological effects of several peptide hormones and growth factors on colon cancer cells have also been documented (Singh et al, 1990), demonstrating interactions between colon cancer and the neuroendocrine system.…”

supporting

confidence: 63%

“…The dose of neurotensin delivered by osmotic pumps for promoting colonic tumor growth in nude mice, 0.54 μmol/kg every 24 hr, is similar to that capable of inducing small intestinal (Chung et al, 1992) or colonic (Evers et al, 1992b) mucosal growth in normal rats. However, the mechanism is probably different since neurotensin promotes tumor cell growth via an NTR1‐mediated event in human colon cancer cells (see above), whereas an unknown indirect mechanism appears to be the predominant action of neurotensin on growth of normal gut mucosa (Chung et al, 1992) in view of the absence of neurotensin receptors in normal intestinal epithelial cells (Laburthe and Amiranoff, 1989; Maoret et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…Receptors or biological effects of several peptide hormones and growth factors on colon cancer cells have also been documented (Singh et al, 1990), demonstrating interactions between colon cancer and the neuroendocrine system. As a general rule, these interactions are present in normal colon and appear to be simply retained in neoplastic colonic tissue (Laburthe and Amiranoff, 1989).…”

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confidence: 99%

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Neurotensin and a non-peptide neurotensin receptor antagonist control human colon cancer cell growth in cell culture and in cells xenografted into nude mice

et al. 1999

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The intestine is a large endocrine organ, but the dependence of colon cancer on hormones remains unknown. We show here that neurotensin, a paracrine/endocrine peptide in the gut, and the neurotensin receptor antagonist SR 48692 control colon cancer cell growth in vitro and in vivo by interacting with receptors that are ectopically expressed in colon cancers. In cell culture, neurotensin stimulates the growth of human colon cancer cell lines (SW480, SW620, HT29, HCT116 and Cl.19A) expressing the neurotensin receptor NTR1 but does not change the growth of Caco2 cells, which do not express NTR1. In SW480 cells, neurotensin is active in the 10–10 to 10–6 M concentration range (ED50 = 0.47 nM) while the neurotensin fragment (1–11) is inactive. Neurotensin also enhances the cellular cloning efficiency of SW480 cells in soft agar by inducing a 50% increase of colony formation. This effect is blocked by SR 48692, which alone does not alter colony formation. Subcutaneous delivery of neurotensin (0.54μmol/kg every 24 hr) by osmotic pumps to nude mice that have been xenografted with SW480 cells results in a significant increase of tumor volume, i.e., up to 255% of control at day 20 of treatment. SR 48692 administered alone (1.7 μmol/kg every 24 hr) by daily i.p. injections reduces the development of tumors formed by xenografting SW480 cells in nude mice. A significant mean reduction of tumor volume of 38% is observed during the 22‐day period of treatment. SR 48692 alone is also active at reducing tumor volume after xenografting HCT116 cells in nude mice. Our results support the notion that colon cancer growth may be dependent on blood‐borne neurotensin and suggest that non‐peptide neurotensin antagonists, such as SR 48692, may be useful for the development of novel therapeutic strategies of colon cancer. Int. J. Cancer 80:448–454, 1999. © 1999 Wiley‐Liss, Inc.

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confidence: 63%

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confidence: 99%

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Neurotensin and a non-peptide neurotensin receptor antagonist control human colon cancer cell growth in cell culture and in cells xenografted into nude mice

et al. 1999

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“…However, this may not explain why different results are obtained using the same cross-linkers (TABLE 1). (3) The use of different biological preparations, for example membranes versus intact cells, may also play a role." Recent experiments performed on membrane-bound and solubilized receptors emphasize the importance of receptor environment and accessibility for cross-linking reactions."…”

mentioning

confidence: 99%

Molecular Analysis of Vasoactive Intestinal Peptide Receptors: A Comparison with Receptors for VIP‐Related Peptides

Laburthe

Couvineau

1988

Annals of the New York Academy of Sciences

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“…VIP was initially isolated from the gut and was later found in the central and peripheral nervous system. It has a n important role in the physiology and physiopathology of the gastrointestinal tract, and its biological effects are mediated via stimulation of cAMP production (Laburthe and Amiranoff, 1989). Recently, VIP has been found to have growth regulatory properties in various cell types.…”

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confidence: 99%

Vasoactive intestinal peptide and forskolin regulate proliferation of the HT29 human colon adenocarcinoma cell line

Gamet

Murat

Rémaury

et al. 1992

Journal Cellular Physiology

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Although several lines of evidence implicate cAMP in the regulation of intestinal cell proliferation, the precise role of this second messenger in the control of the human colon cancer cell cycle is still unclear. In order to investigate the role of cAMP in HT29 cell proliferation, we have tested the effect of vasoactive intestinal peptide (VIP) and forskolin on DNA synthesis and cell number, focusing on the time-dependent efficacy of the treatment. The cells were arrested in G0/G1 phase by incubation for 24 h in serum-free medium and proliferation was re-initiated by addition of either 85 nM insulin or 0.5% fetal calf serum. In the presence of fetal calf serum, G1/S transition was found to occur earlier than with insulin. Exposure of the HT29 cells to 10(-5) M forskolin in the early stages of growth induction (within 12 h from FCS addition or within 14 h from insulin treatment) resulted in a significant inhibition of DNA synthesis and a delayed entry in the S phase. By contrast, VIP (10(-7) M) was inhibitory only when added within a narrow window (10 to 12 h or 12 to 14 h following FCS or insulin addition, respectively). The difference in efficiency of forskolin and VIP to inhibit cell proliferation may be correlated with their own potency to promote long-lasting cAMP accumulation. The combination of VIP plus forskolin had synergistic effects on both cAMP accumulation and cell-growth inhibition. Taken together, our data indicate that cAMP may act at a step in the late G1 or G1/S transition.

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Peptide Receptors in Intestinal Epithelium

Cited by 12 publications

References 333 publications

Neurotensin and a non-peptide neurotensin receptor antagonist control human colon cancer cell growth in cell culture and in cells xenografted into nude mice

Neurotensin and a non-peptide neurotensin receptor antagonist control human colon cancer cell growth in cell culture and in cells xenografted into nude mice

Molecular Analysis of Vasoactive Intestinal Peptide Receptors: A Comparison with Receptors for VIP‐Related Peptides

Vasoactive intestinal peptide and forskolin regulate proliferation of the HT29 human colon adenocarcinoma cell line

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