Enhancement by vaso‐active intestinal peptide of gastric carcinogenesis induced by N‐methyl‐N'‐nitro‐N‐nitrosoguanidine in rats

Abstract

The effects of vaso-active intestinal peptide (VIP) on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats given VIP every other day for 27 weeks after oral administration of MNNG for 25 weeks. In week 52, administration of VIP caused a significant increase in the incidence of gastric cancers, but did not influence their histological appearance. VIP significantly increased the labeling indices of the antral mucosa. Our findings indicate that VIP enhances gastric carcinogenesis, and that this effect may be related to its effect in increasing cell proliferation of the antral epithelial cells.

Inhibition by amiloride of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats

“…Similarily, we previously reported that prolonged administration of tyrosine methyl ester, neurotensin and vasoactive intestinal peptide significantly increased the labelling index of the antral cells, but they had little or no influence on the labelling index of the fundic epithelial cells (Tatsuta et al, 1989d(Tatsuta et al, , 1991Iishi et al, 1992). However, the reason why the fundus and antrum differ is not known.…”

Effect of vasoactive intestinal peptide on gastric adenocarcinoma

“…It is not clear if the autocrine regulation of VIP in gastric cancer cells exists and if so, how it affects gastric cancer cells. Kim reported the VIP inhibited the growth of AGS gastric cancer cells by inhibiting c‐myc expression in vitro , 17 but Iishi reported that VIP enhanced the development of rat gastric cancer induced by MNNG in vivo, 18 so we speculated that gastric cancer cells might exist in the autocrine regulation of VIP.…”

“…The physiological functions of VIP in the GI tract are associated with the secretion and motor of the digestive system. Recently, many studies showed that VIP was closely correlated with malignancy, 6–18 and some studies showed that VIP also had close correlation with gastric cancer, but some controversies and questions still exist.…”

“…Reubi and Virgolini found there were VIPR in 54–100% of gastric cancer tissues, 5,6,16 but those receptors were not tested to see if they derived from cancer cells or interstitial cells. Kim reported the VIP inhibited the growth of AGS gastric cancer cells by inhibiting c‐myc expression in cells, 17 but Iishi reported that VIP enhanced the development of rat gastric cancer induced by N‐methyl‐N′‐nitro‐N‐ nitrosoguanidine (MNNG) 18 . Although little is known as to whether gastric cancer cells secrete VIP and exist in the autocrine regulation of VIP, we reasonably suppose that gastric cancer cells can express VIP and its receptors, and exist in the autocrine regulation of VIP.…”