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A Selective Cyclooxygenase‐2 Inhibitor Suppresses Tumor Growth in Nude Mouse Xenografted with Human Head and Neck Squamous Carcinoma Cells

机译:一种选择性的环氧合酶-2抑制剂抑制人头颈部鳞状细胞癌异种移植裸鼠的肿瘤生长。

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摘要

The anti‐tumor effect of a selective cyclooxygenase (COX)‐2 inhibitor, JTE‐522, was examined with the human head and neck squamous cell carcinoma cell line KB. KB cells do not produce prostaglandin (PG)‐E2. In vitro, JTE‐522 induced an increase of G1 phase‐arrested cells, suppression of platelet‐derived growth factor (PDGF) production and inhibition of telomerase activity. No cytotoxic effect was detected. In vivo, the growth of the tumor xenografted into nude mice was significantly suppressed by JTE‐522. Suppression of angiogenesis at the periphery of the tumor, increase of G1‐arrested cells and suppression of telomerase activity were observed, together with an increase of apoptotic cell death in the tumor. Immunological enhancement did not play a role. We concluded that the anti‐tumor effect of JTE‐522 was caused by anti‐angiogenesis action, cell cycle arrest and inhibition of telomerase activity of the tumor cells. These combined effects might induce apoptosis.
机译:选择性环氧化酶(COX)-2抑制剂JTE-522的抗肿瘤作用已通过人头颈部鳞状细胞癌细胞系KB进行了检验。 KB细胞不产生前列腺素(PG)-E2。在体外,JTE-522诱导了G1期阻滞细胞的增加,抑制了血小板衍生生长因子(PDGF)的产生并抑制了端粒酶活性。未检测到细胞毒性作用。在体内,JTE-522显着抑制了异种移植到裸鼠体内的肿瘤的生长。观察到肿瘤周围血管生成的抑制,G1阻滞细胞的增加和端粒酶活性的抑制,以及肿瘤中凋亡细胞死亡的增加。免疫增强作用不起作用。我们得出结论,JTE-522的抗肿瘤作用是由抗血管生成作用,细胞周期阻滞和肿瘤细胞端粒酶活性的抑制引起的。这些综合作用可能诱导凋亡。

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