2013
DOI: 10.1155/2013/429545
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Effect of Vasoactive Intestinal Peptide (VIP) on NKG2D Signal Pathway and Its Contribution to Immune Escape of MKN45 Cells

Abstract: Objective. To investigate VIP effect on the cytotoxicity of NK cell to gastric cancer cells in vitro and the relation between the effect with the NKG2D signal molecules in NK cells. Material and Methods. NK cells were purified from peripheral blood mononuclear cells (PBMC). Before and after NK cells were incubated with VIP or its antagonist (D-p-Cl-Phe6,Leu17)-VIP, we detected the cytotoxicity of NK cells to MKN45 gastric cancer cells by MTT and detected the expressions of NKG2D, DAP10, and NF-κB proteins and … Show more

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Cited by 6 publications
(5 citation statements)
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“…Secondly, we hypothesized that phytoncides are able to stimulate the olfactory epithelium and regulate hormones. Among these hormones, vasoactive intestinal peptide (VIP) is known to be able to control NK cell activation [ 59 , 60 ].…”
Section: Discussionmentioning
confidence: 99%
“…Secondly, we hypothesized that phytoncides are able to stimulate the olfactory epithelium and regulate hormones. Among these hormones, vasoactive intestinal peptide (VIP) is known to be able to control NK cell activation [ 59 , 60 ].…”
Section: Discussionmentioning
confidence: 99%
“…It is well established that cell transformation results in increased NKG2DL expression in relation to their basal levels, thus converting these cells in a specific target for NK cell-mediated cytotoxicity, which may determine their elimination ( 8 , 9 ). However, high MICA and MICB expression in the primary tumor tissue may provide a selective advantage for tumor cells that sustain MICA and MICB expression and, instead of immune activation, this prevalent expression would promote immune suppression, since persistent NKG2DL expression may desensitize NK cells and render them dysfunctional, which is a determinant of tumor aggressiveness ( 21 , 46 , 47 ). However, it is worth mentioning that other factors, such as soluble NKG2DLs ( 19 ) and TGF-β released from tumors ( 48 ), may more strongly impair NK cell and other lymphocytes cytotoxicity, compromising their function and favoring malignant progression.…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, targeting CXCR2 may represent a novel therapeutic strategy for breast cancers. Other genes, such as vasoactive intestinal polypeptide (VIP) could inhibit the cytotoxicity of NK cells and could inhibit its expressions of some immune-associated genes like NKG2D and NF-κB [53]. Neurotensin (NTS) belong to Neuropeptide G protein-coupled receptors (GPCRs) are over-expressed in numerous cancer cells and were reported to stimulate tumor growth [54].…”
Section: Discussionmentioning
confidence: 99%