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Objective: To observe the vasoactive intestinal peptide (vasoactive intestinal peptide, VIP) in gastric cancer and adjacent normal tissues, NK cell activation lectin-like receptor homodimer (natural killer group 2, member D, NKG2D) and its associated signaling molecules adapter protein 10 (adaptor protein 10, DAP 10) phosphatidylinositol 3-kinase (phosphatidylinositol 3 kinase, PI3K) and nuclear factor-κB (nuclear factor-kappa B, NF-κB) in gastric cancer and adjacent normal tissue expression of inflammatory cells, gastric carcinoma VIP preliminary analysis of inflammatory cells with the corresponding NKG2D and its associated signaling molecules to each other. Methods: First Affiliated Hospital of Nanchang University, September 2008 - June 2009 clinical gastric cancer surgery, adjacent normal tissues and 72 cases of clinical and pathological data. Including 52 males and 20 females, aged 40 to 83 years, mean age 60.4 ± 11.4 years old. 40-60 years 34 cases, gt; 60 years 38 cases; gastric lesions in 44 cases, 28 cases of gastric body; postoperative pathology suggestive of lymph node metastasis in 44 cases, 28 cases without lymph node metastasis; highly differentiated in 24 cases, low Differentiation of 48 cases; and based on pathological findings in accordance with the TNM staging, TNM stage Ⅰ, Ⅱ stage were a total of 30 cases, Ⅲ - Ⅵ term, a total of 42 cases. Immunohistochemistry was used to detect the cancer tissue, adjacent normal tissue expression of VIP, the corresponding inflammatory cells NKG2D, DAP10, PI3K and NF-κB protein expression. Results: 1, VIP in gastric cancer tissues and adjacent normal tissues were 96% and 89%; former than the latter, but there was no significant difference (P gt; 0.05). The VIP in gastric cancer tissues was significantly higher than intensity of adjacent normal tissues (P lt; 0.05). VIP expression in gastric cancer strength, poorly differentiated, lymph node metastasis, clinical stage Ⅲ - Ⅳ stage patients was significantly stronger than the high school division, without lymph node metastasis and clinical stage Ⅰ - Ⅱ stage patients (P lt; 0.05). However, different gender, different age groups and between different lesions, gastric tissue expression of VIP was no significant difference (P gt; 0.05). 2, NKG2D inflammatory cells in gastric carcinoma and adjacent normal tissue inflammatory cells were 44% and 96%; former than the latter, both of which there was a significant difference between (P lt; 0.01). NKG2D in gastric intensity of inflammatory cells was significantly lower than in adjacent normal tissue inflammatory cells (P lt; 0.01). Inflammatory cells in the gastric NKG2D expression intensity, poor differentiation, lymph node metastasis, clinical stage Ⅲ - Ⅳ stage patients was significantly weaker than the high grade group without lymph node metastasis and clinical stage Ⅰ - Ⅱ stage patients (P lt ; 0.05). However, different gender, different age groups and between different lesions, inflammatory cells in the gastric tissue expression of NKG2D was no significant difference (P gt; 0.05). 3, DAP10 inflammatory cells in gastric carcinoma and adjacent normal tissue inflammatory cells were 50% and 92%; former than the latter, and between the two there was a significant difference (P lt; 0.01). DAP10 in gastric intensity of inflammatory cells was significantly lower than in adjacent normal tissue inflammatory cells (P lt; 0.01). Inflammatory cells in the gastric DAP10 expression intensity, moderately differentiated group without lymph node metastasis, Ⅰ - Ⅱ clinical staging of patients was significantly stronger than the poorly differentiated group with lymph node metastasis and clinical stage Ⅲ - Ⅳ stage patients (P lt; 0.05). However, different gender, different age groups and between different lesions, inflammatory cells in the gastric DAP10 expression intensity was no significant difference (P gt; 0.05). 4, PI3K p85a inflammatory cells in gastric carcinoma and adjacent normal tissue inflammatory cells were 31% and 71%; former than the latter, both of which there was a significant difference between (P lt; 0.01). PI3Kp85a in gastric intensity of inflammatory cells was significantly lower than in adjacent normal tissues (P lt; 0.01). Inflammatory cells in the gastric tissue expression of PI3K p85α strength, poor differentiation, lymph node metastasis, clinical stage Ⅲ - Ⅳ stage patients was significantly weaker than the high grade group without lymph node metastasis and clinical stage Ⅰ - Ⅱ stage patients (P lt; 0.05). However, different gender, different age groups and between different lesions, inflammatory cells in the gastric tissue expression of PI3K was no significant difference (P gt; 0.05). 5, NF-κB p65 in gastric inflammatory cells and normal tissue inflammatory cells were 57% and 86%; former was significantly lower than the latter (P lt; 0.01), NF-κB p65 in Gastric intensity of inflammatory cells was significantly lower than in adjacent normal tissue inflammatory cells (P lt; 0.01). Inflammatory cells in the gastric NF-κB p65 expression intensity, poor differentiation, lymph node metastasis, clinical stage Ⅲ - Ⅳ stage patients was significantly weaker than the high grade group without lymph node metastasis and clinical stage Ⅰ - Ⅱ stage patients (P lt; 0.05). However, different gender, different age groups and between different lesions, inflammatory cells in the gastric NF-κB p65 expression intensity was no significant difference (P gt; 0.05). 6, gastric carcinoma VIP protein expression and inflammatory cells in gastric cancer tissues NKG2D, DAP10, PI3K p85α, NF-κB p65 protein expression was significantly negatively correlated with intensity of (P lt; 0.05). Conclusion: VIP in gastric cancer tissues was significantly higher than the intensity of adjacent normal tissue; while NKG2D, DAP10, PI3Kp85α, NF-KBp65 inflammatory cells in gastric cancer tissues was significantly lower than in the expression of inflammatory cells in adjacent tissues. VIP cancer tissue expression of inflammatory carcinoma cells NKG2D, DAP10, PI3Kp85α, NF-KBp65 a significantly negative correlation expression. VIP possibly through inhibition of immune cells NKG2D/DAP10/PI3K/NF-κB pathway, inhibition of immune surveillance, and promote gastric cancer immune escape.
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