FABP4 accelerates colon cancer cells metastasis by promoting GLUTI expression and Aerobic glycolysis
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摘要:
目的：探讨脂肪酸转运蛋白4（fatty acid binding protein 4，FABP4）在肠癌细胞侵袭转移中的作用和机制。方法：通过ELISA和Western blot检测不同侵袭转移能力肠癌细胞中FABP4表达水平；采用Transwell实验检测肠癌细胞侵袭转移能力；使用siRNA技术干扰HT29细胞中葡萄糖转运蛋白1（glucose transporter 1，GLUT1）表达，检测肠癌细胞葡萄糖摄取、乳酸脱氢酶含量、乳酸生成水平。结果：在高转移性肠癌细胞系HTCC116、SW620、Lovo的培养基上清和细胞中，FABP4表达显著高于低转移性肠癌细胞系HT29、Colo-2、SW116。用hrFABP4处理的HT29，其侵袭能力增强；而用FABP4抑制剂BMS处理的HTC116，其侵袭能力被明显抑制。过表达hrFABP4促进肠癌细胞中GLUT1的表达和有氧糖酵解。下调GLUT1或抑制有氧糖酵解能够削弱hrFABP4引起的肠癌细胞侵袭和转移。结论：FABP4可促进肠癌细胞侵袭转移，其机制可能通过促进GLUT1表达，进而诱导有氧糖酵解。
Abstract:
Objective：To explore the role of fatty acid binding protein 4（FABP4）in colon cancer cell invasion. Methods：The expression of FABP4 in a panel of colon cancer cell lines was detected by ELISA and Western blot. Transwell assays were performed to determine invasion of colon cancer cells. The glucose transporter 1（GLUT1）expression in HT29 cell was knockdown by siRNA and glucose uptake. LDH level and lactate production of colon cancer cells were analysed. Results：The expression of FABP4 in medium supernatant and cells was increased in colcon cancer cells HTCC116，SW620 than that in HT29，Colo-2 and SW116 cells. Overexpression of hrFABP4 promoted invasion in HT29 cells，whereas inhibitor of FABP4 impaired the invasion rate of HTC116 cells. The expression of GLUT1 and aerobic glycolysis of colon cancer cells were upregulated by hrFABP4. Knockdown of GLUT1 or inhibition of aerobic glycolysis in HT29 cell abrogated the effect of hrFABP4 on cell invasion. Conclusion：FABP4 may promotes invasion in colon cancer cells through upregulation of GLUT1 and increased aerobic glycolysis.
