Cephalosporium curvulum lectin (CSL), a lectin from pathogenic fungus has exquisite specificity towards α1–6 linkage of core fucosylated glycans, expressed in hepatocellular and pancreatic cancer. Interaction and effect of CSL and other fucose specific lectins LCA and AOL on HepG2 and PANC-1 cells was investigated. CSL, LCA and AOL exhibited strong binding to PANC-1 cells which could be effectively blocked by competing glycoprotein mucin. Effect of CSL, LCA and AOL on PANC-1 and HepG2 cells was determined by MTT assay and all the three lectins inhibited the cell growth which could be blocked by mucin, cell cycle analysis revealed that CSL increased hypodiploid HepG2 cell population indicating cellular apoptosis. CSL induced apoptosis in HepG2 cells was confirmed by Annexin V/PI assay. CSL induced increase in early apoptotic HepG2 cell population, a time dependent increase in the expression of caspases-3, 9 and cytochrome-c was observed by western blotting suggesting the possible involvement of intrinsic caspase dependent apoptosis. Increase in ROS and decrease in MMP demonstrated involvement of intrinsic caspase dependent apoptosis. Quantification of AFP in HCC patients using CSL lectin-antibody sandwich ELISA, supports diagnostic potential of CSL.

中文翻译：

---

弯曲头孢霉的核心岩藻糖特异性凝集素诱导肝细胞和胰腺癌细胞的细胞凋亡，并有效检测AFP。

头孢菌凝集素（CSL）是一种来自致病性真菌的凝集素，对在肝细胞癌和胰腺癌中表达的岩藻糖基化核心聚糖的α1–6连接具有极高的特异性。研究了CSL和其他岩藻糖特异性凝集素LCA和AOL对HepG2和PANC-1细胞的相互作用和效应。CSL，LCA和AOL与PANC-1细胞具有很强的结合力，可以被竞争性糖蛋白粘蛋白有效地阻断。MTT法测定了CSL，LCA和AOL对PANC-1和HepG2细胞的影响，所有三种凝集素均抑制了粘蛋白可能阻断的细胞生长，细胞周期分析表明CSL增加了二倍体HepG2细胞群，表明细胞凋亡。通过膜联蛋白V / PI测定证实了CSL诱导的HepG2细胞凋亡。CSL诱导早期凋亡的HepG2细胞数量增加，通过蛋白质印迹观察到caspases-3、9和细胞色素c的表达随时间的增加，这提示可能涉及内在的半胱天冬酶依赖性凋亡。ROS的增加和MMP的减少表明内在的半胱天冬酶依赖性凋亡。使用CSL凝集素-抗体夹心ELISA对HCC患者的AFP进行定量分析，具有CSL的诊断潜力。