Promotion by substance P of gastric carcinogenesis induced by N-methyl-N′-nitro-N-nitrosoguanidine in Wistar rats

Tatsuta, Masaharu; Baba, Miyako; Yano, Hiroyuki; Iseki, Kazushige; Uehara, Hiroyuki; Nakaizumi, Akihiko

doi:10.1016/0304-3835(95)03917-l

Cited by 14 publications

(9 citation statements)

References 21 publications

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“…Especially, SP was associated with differentiation of gastric cancer and promoted proliferation, adhesion, migration, and invasion of gastric cancer cells [13]. Moreover, long-term administration of SP significantly increased the incidence of gastric cancer in week 52 [14]. In present study, we demonstrated that SP promotes the development of gastric cancer by increasing cell viability and suppressing apoptosis in gastric cancer cells, which is consistent with previous studies.…”

Section: -1-ig)supporting

confidence: 92%

“…Besides, in vitro studies have demonstrated that SP promoted the proliferation, adhesion, migration, and invasion in human gastric cancer cells [13]. Meanwhile, in vivo studies indicated that a significant increase in the incidence of gastric cancer was observed after long-term injection of SP in Wistar rats [14]. Therefore, SP plays a promoting role in the development of gastric cancer.…”

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confidence: 99%

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miR-877-5p antagonizes the promoting effect of SP on the gastric cancer progression

Guo¹,

Zhang²,

Sha³

2021

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Gastric cancer is one of the four major tumors in the world and the second leading cause of cancer-related death. It was reported that Substance P (SP), as an oncogenic factor, could regulate the expression of miRNAs in gastric cancer progression. Here, we focused on the role of miR-877-5p in gastric cancer development and the miR-877-5p involvement in the SP-mediated gastric cancer development. The mRNA expression level and cell proliferation were assessed by quantitative real-time PCR and cell counting kit-8 assay, respectively. Flow cytometry was conducted to detect apoptosis, followed by assessing the expression of related apoptosis factors. Dual-luciferase reporter assay was performed to validate the interaction between miR-877-5p and Forkhead cassette M1 (FOXM1). Our results showed that SP treatment significantly increased cell proliferation in gastric cancer. Moreover, the miR-877-5p expression was dose-dependently decreased by SP, whereas FOXM1 expression was markedly increased by SP in gastric cancer cells. miR-877-5p negatively regulated gastric cancer development via inhibiting cell p roliferation and promoting apoptosis accompanied by increased cleaved caspase-3, cleaved caspase-9, and bax protein levels and decreased bcl-2 level. We confirmed that miR-877-5p could target FOXM1 and negatively regulate its expression. Furthermore, we demonstrated that SP could promote cell proliferation and inhibit apoptosis, while miR-877-5p overexpression reversed the effect of SP on cell proliferation and apoptosis. These results suggest that miR-877-5p overexpression can antagonize the promoting effect of SP on the development of gastric cancer, indicating that miR-877-5p may serve as a promising therapeutic target for gastric cancer.

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Section: -1-ig)supporting

confidence: 92%

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confidence: 99%

miR-877-5p antagonizes the promoting effect of SP on the gastric cancer progression

Guo¹,

Zhang²,

Sha³

2021

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“…Repeated administration of capsaicin suppressed the flare response in human skin by depleting the neuronal release of a pro-inflammatory mediator Substance P (34). Capsaicin-induced depletion of Substance P, which acts as a tumor promoter (35), may underlie the protective effects of the compound against of N-methyl-N'-nitro-N-nitrosoguanidin (MNNG)-initiated gastric carcinogenesis. A major cause of gastric carcinogenesis is Helicobacter pylori infection.…”

Section: Modulation Of Cellular Detoxification and Antioxidant Capacitymentioning

confidence: 99%

An updated review on molecular mechanisms underlying the anticancer effects of capsaicin

Cho

Lee

Choi

2017

Food Sci Biotechnol

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The quest for developing anticancer principles from natural sources has a long historical track record and remarkable success stories. The pungent principle of hot chili pepper, capsaicin, has been a subject of research for anticancer drug discovery for more than three decades. However, the majority of research has revealed that capsaicin interferes with various hallmarks of cancer, such as increased cell proliferation, evasion from apoptosis, inflammation, tumor angiogenesis and metastasis, and tumor immune escape. Moreover, the compound has been reported to inhibit carcinogen activation and chemically induced experimental tumor growth. Capsaicin has also been reported to inhibit the activation of various kinases and transcription that are involved in tumor promotion and progression. The compound activated mitochondria-dependent and death receptor-mediated tumor cell apoptosis. Considering the growing interest in capsaicin, this review provides an update on the molecular targets of capsaicin in modulating oncogenic signaling.

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“…The administration of high doses of SP favors gastric carcinogenesis induced by N-methyl-N′-nitro-N-nitrosoguanidine, this effect being associated with the stimulation of the proliferation of antral epithelial cells. [ 22 ] Myenteric denervation decreases the number and size of gastric adenocarcinomas, this decrease being more evident when denervation is associated with pyloroplasty. [ 23 ] The authors of an in vitro study have reported that SP promotes proliferation, adhesion, migration, and invasion of MKN45 gastric cancer cells.…”

Section: The Substance P/nk-1 Receptor System In Gi Cancermentioning

confidence: 99%

Neurokinin-1 receptor antagonists as antitumor drugs in gastrointestinal cancer: A new approach

Muñoz

Coveñas

2016

Saudi J Gastroenterol

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Gastrointestinal (GI) cancer is the term for a group of cancers affecting the digestive system. After binding to the neurokinin-1 (NK-1) receptor, the undecapeptide substance P (SP) regulates GI cancer cell proliferation and migration for invasion and metastasis, and controls endothelial cell proliferation for angiogenesis. SP also exerts an antiapoptotic effect. Both SP and the NK-1 receptor are located in GI tumor cells, the NK-1 receptor being overexpressed. By contrast, after binding to the NK-1 receptor, NK-1 receptor antagonists elicit the inhibition (epidermal growth factor receptor inhibition) of the proliferation of GI cancer cells in a concentration-dependent manner, induce the death of GI cancer cells by apoptosis, counteract the Warburg effect, inhibit cancer cell migration (counteracting invasion and metastasis), and inhibit angiogenesis (vascular endothelial growth factor inhibition). NK-1 receptor antagonists are safe and well tolerated. Thus, the NK-1 receptor could be considered as a new target in GI cancer and NK-1 receptor antagonists (eg, aprepitant) could be a new promising approach for the treatment of GI cancer.

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Promotion by substance P of gastric carcinogenesis induced by N-methyl-N′-nitro-N-nitrosoguanidine in Wistar rats

Cited by 14 publications

References 21 publications

miR-877-5p antagonizes the promoting effect of SP on the gastric cancer progression

miR-877-5p antagonizes the promoting effect of SP on the gastric cancer progression

An updated review on molecular mechanisms underlying the anticancer effects of capsaicin

Neurokinin-1 receptor antagonists as antitumor drugs in gastrointestinal cancer: A new approach

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