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阿司匹林、舒林酸对3AO细胞环氧合酶-2、血管生长因子、层粘蛋白受体、CD_(44)V_6表达的影响

Effects of aspirin and sulindac on expression of cyclooxygenase-2, vascular endothelial growth factor, laminin receptor, and CD_(44)V_6 in 3AO cells
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摘要 目的 :研究阿司匹林、舒林酸对 3AO细胞环氧合酶 2 (COX 2 )、血管生长因子 (VEGF)、CD44V6及层粘蛋白受体 (LN R)表达的影响。方法 :采用MTT方法观察阿司匹林、舒林酸在贴壁前后加入培养液中对 3AO细胞生长的影响。采用免疫细胞化学的方法研究两种药物对 3AO细胞COX 2、VEGF、CD44V6、LN R的影响。结果 :MTT实验显示阿司匹林、舒林酸不论在贴壁前还是后加入均可抑制 3AO卵巢癌细胞的生长 ,加药后调节pH可减弱生长抑制作用但仍然可明显抑制肿瘤细胞的生长。阿司匹林和舒林酸对COX 2、VEGF的表达也有抑制作用 ,但对CD44V6及LN R的表达无明显影响。结论 :抑制COX 2的表达可以下调VEGF的表达 ,从而抑制肿瘤的血管生成。阿司匹林和舒林酸可通过抑制COX 2及VEGF的表达而抑制肿瘤的生长。 AIM: To investigate the effects of aspirin and sulindac on the expression of cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), CD 44V 6 and laminin receptor (LN-R) in 3AO cells. METHODS: The growth inhibition effects of aspirin and sulindac in 3AO cells were tested by MTT assay. The expression of COX-2, VEGF, LN-R and CD 44V 6 were evaluated by immunocytochemistry. RESULTS: Aspirin and sulindac significantly inhibited the growth of 3AO cells whether added before or after cells adhered. When the pH was adjusted with sodium bicarbonate, the inhibition had a little decrease. Aspirin and sulindac also inhibited the expression of COX-2 and VEGF. But there were no effect on the expression of LN-R and CD 44V 6. CONCLUSION: Inhibited expression of COX-2 may down-regulate the expression of VEGF, and inhibit the angiogenesis of tumor. Aspirin and sulindac may exert their chemopreventive and anticancer effects by inhibiting the expressions of COX-2 and VEGF.
出处 《中国临床药理学与治疗学》 CAS CSCD 2004年第8期906-910,共5页 Chinese Journal of Clinical Pharmacology and Therapeutics
基金 山东省卫生厅青年基金资助项目 (№ 1999CA2CACA1)
关键词 阿司匹林 舒林酸 COX-2 VEGF CD44V6 LN-R aspirin sulindac cyclooxygenase-2 vascular endothelial growth factor laminin receptor CD_(44)V_6
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  • 1[1]Sandler RS, Glanko JC, Murray SC, Helm JF, Woosley JT.Aspirin and non steroidal anti-inflammatory agents and risk for colorectal adenomas[J]. Gastroenerology, 1998; 114 (30): 441-7
  • 2[2]Castelao JE, Yuan JM, Gago-Dominguez M , Yu MC, Ross RK. Non-steroids anti-inflamatory drugs and bladder cancer prevention [J]. Br J Cancer, 2000;82(7): 1364 - 9
  • 3[3]Norrish AE, Jackson RT, Mcrae CU. NSAIDs and prostate cancer prevention [J]. Int J Cancer, 1998;77(4) :511 - 5
  • 4[4]Harris RE, Beebe-Donk J, Namboodiri KK. Inverse association of non steroidal anti-inflammatory drugs and malignant melanoma among woman[J]. Oncol Rep, 2001 ;8(3) :655 - 7
  • 5[5]Smalley W, Ra WA, Daugherty J, Griffin MR. Use of non-steroidal anti-inflammatory drug and incidence of colorectal cancer.A population study [J]. Arch Intern Med, 1999; 159(2): 161-6
  • 6[6]Dohadwala M, Batra RK, Luo J, Lin Y, Krysan K, Pold M, et al. Autocrine/paracrine prostaglandin E2 production by nonsmall cell lung cancer cells regulates matrix metalloproteinase-2and CD44 in cyclooxygenase-2-dependent invasion [J]. J Biol Chem, 2002;277(52) :50828 - 33
  • 7[7]Liu LT, Chang HC, Chiang LC, Hung WC. Induction of RECK by nonsteroidal anti-inflammatory drugs in lung cancer cells [J]. Oncogene, 2002;21(54) :8347 - 50
  • 8[8]Li G, Yang T, Yan. Cyclooxygenase-2 increased the angiogenic and metastatic potential of tumor cells[J]. Biochem Biophys Res Commun, 2002;299(5) :886 - 90
  • 9[9]Niki T, Kohno T, Iba S, Moriya Y, Takahashi Y, Saito M, et al. Frequent co-localization of COX-2 and laminin-5 gamma2chain at the invasive front of early-stage lung adenocarcinomas [J]. AmJ Pathol, 2002;160(3):1129-41
  • 10[10]Dormond O, Bezzi M, Mariotti A, Ruegg C. Prostaglandin E2promotes integrin alpha V beta 3-dependent endothelial cell adhesion, rac-activation, and spreading through cAMP/PKA-dependent signaling[J]. J Biol Chem, 2002; 277(48):45838-46

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