本文選題：腺樣囊性癌 + 免疫組化��； 參考：《廣西醫(yī)科大學》2014年碩士論文

【摘要】：目的： 研究靶向抑制CXCR4對耐藥腺樣囊性癌細胞系移植瘤中的P-gp，VEGFR2，Ki-67的表達，探討CXCR4對耐藥腺樣囊性癌生物學特性的影響。 方法： （1）在脂質體介導下，將靶向CXCR4基因的shRNA真核表達載體質粒體外轉染腺樣囊性癌耐藥細胞系NACC-DDP，轉染細胞建立裸鼠腮腺移植瘤，觀察成瘤情況。 （2）實驗將裸鼠分為非轉染組、空載體、陰性質粒對照組、shCXCR4組。接種后第35天處死動物，制備病理切片。 (3)通過組織切片脫蠟,水化,高壓熱修復,阻斷過氧化物酶,滴加P-gp(1:200),VEGFR2(1:50),Ki-67等抗體,滴加生物素標記二抗工作液,滴加辣根酶標記的鏈霉卵白素工作液,DAB顯色,蘇木素復染,樹膠封片等免疫組織化學法檢測P-gp，VEGFR2，，Ki-67表達的情況。 結果： 1. P-gp,VEGFR2主要表達于胞漿。分析結果顯示，非轉染組，空載體組，陰性質粒對照組P-gp,VEGFR2陽性表達率均高于shCXCR4組,差異有統(tǒng)計學意義(P0.05)。 2.Ki-67主要表達于細胞核。分析結果顯示，非轉染組，空載體組，陰性質粒對照組Ki-67陽性表達率高于shCXCR4組，差異有統(tǒng)計學意義(P0.05)。 結論： 下調CXCR4基因的NACC-DDP細胞移植瘤生長明顯減慢，P-gp、VEGFR2、Ki-67表達明顯降低，提示干擾CXCR4基因的表達可抑制耐藥腺樣囊性癌的增殖；下調耐藥蛋白表達；并具有抗腫瘤血管生成的效應。CXCR4可望成為靶向抑制腺樣囊性癌的靶點
[Abstract]:Objective: To investigate the effect of CXCR4 on the biological characteristics of drug-resistant adenoid cystic carcinoma (ADSCC), to investigate the inhibitory effect of CXCR4 on the expression of P-gptVEGFR2KI-67 in drug-resistant adenoid cystic carcinoma cell line transplantation and to investigate the effect of CXCR4 on the biological characteristics of drug-resistant adenoid cystic carcinoma. Methods: The adenoid cystic carcinoma resistant cell line NACC-DDP was transfected with shRNA eukaryotic expression vector plasmid targeting CXCR4 gene in vitro, and the xenograft tumor of parotid gland in nude mice was established by transfection of NACC-DDP. The nude mice were divided into three groups: non-transfection group, empty vector group and negative plasmid control group (shCXCR4). On the 35th day after inoculation, the animals were killed and pathological sections were prepared. (3) through tissue section dewaxing, hydration, high pressure thermal repair, blocking peroxidase, dripping with antibodies P-gp1: 1: 1: 1: 1: 50 + Ki-67, adding biotin-labeled second antibody working fluid, drip adding horseradish enzyme labeled streptavidin working fluid DAB, hematoxylin restaining, Immunohistochemical method was used to detect the expression of VEGFR2 Ki-67. Results: 1. VEGFR2 was mainly expressed in cytoplasm. The results showed that the positive expression rate of P-gpfR2 in non-transfection group, empty vector group and negative plasmid control group was higher than that in shCXCR4 group, and the difference was statistically significant (P 0.05). 2.Ki-67 is mainly expressed in the nucleus. The results showed that the positive expression rate of Ki-67 in non-transfection group, empty vector group and negative plasmid control group was higher than that in shCXCR4 group, and the difference was statistically significant (P 0.05). Conclusion: The growth of NACC-DDP cells with down-regulation of CXCR4 gene was significantly decreased, and the expression of P-gpCV-VEGFR2Ki-67 was significantly decreased, suggesting that interfering with the expression of CXCR4 gene could inhibit the proliferation of drug-resistant adenoid cystic carcinoma and down-regulate the expression of drug-resistant protein. CXCR4 is expected to be a target for the inhibition of adenoid cystic carcinoma.
【學位授予單位】：廣西醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R739.8

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