探讨非甾体抗炎药对瘦素促结肠癌生长转移作用的抑制及其机制

Non-steroidal Anti-inflammatory Drugs on Leptin Promote Colon Cancer Growth Inhibition of Transfer Function and Its Mechanism

目的:通过观察非甾体抗炎药,舒林酸及塞来昔布对瘦素结肠癌HT-29细胞株c-mycm RNA的影响。方法:体外分组培养结肠癌细胞株HT-29分别与不同浓度的瘦素、舒林酸以及塞来昔布作用后,尚未出现显著细胞杀灭作用的NSAIDs临界药物浓度;逆转录多聚酶链反应(RT-PCR)检测各浓度瘦素组以及上述有效浓度的瘦素、临界药物浓度NSAIDs共同作用组细胞c-mycm RNA、VEGFm RNA表达情况。结果:在瘦素作用下,HT-29细胞的增殖水平及c-mycm RNA、VEGFm RNA表达水平较对照组明显升高并呈现浓度依赖趋势。结论:瘦素能够促进结肠癌HT-29细胞株的增殖并使该细胞株c-myc、VEGF基因的表达水平明显升高;无显著细胞杀灭作用浓度的NSAIDs即能够有效的抑制瘦素作用,抑制了结肠癌细胞的生长及转移。

Objective： by observing the non-steroidal anti-inflammatory drugs, sulindac and celecoxib on leptin HT- 29 colon cancer cell lines c- myc m RNA. Methods： in vitro cultivation of colon cancer cell line HT- 29 respectively with different concentrations of leptin, sulindac and celecoxib, there have been no significant cell killing effect of NSAIDs critical drug concentration; Reverse transcription polymerase chain reaction（rt-pcr） polymer to detect the concentration of leptin groups, and the effective concentration of leptin, the combination of the critical concentration of drugs NSAIDs group cell c- myc m RNA, VEGF m RNA expression. Results：under the effect of leptin, the HT- 29 cell proliferation level and c- myc m RNA, VEGF m RNA expression level was significantly increased and showed a trend of concentration dependence. Conclusion： leptin can promote colon cancer HT- 29 cell line proliferation and the cell lines- myc, the expression level of VEGF gene.