School of Life Sciences & State Key Laboratory of Oral Diseases, Sichuan University, Chengdu 610064, China.
Biochem Biophys Res Commun. 2011 Oct 22;414(2):282-6. doi: 10.1016/j.bbrc.2011.09.072. Epub 2011 Sep 17.
Concanavalin A (ConA), a Ca(2+)/Mn(2+)-dependent and mannose/glucose-binding legume lectin, has drawn a rising attention for its remarkable anti-proliferative and anti-tumor activities to a variety of cancer cells. ConA induces programmed cell death via mitochondria-mediated, P73-Foxo1a-Bim apoptosis and BNIP3-mediated mitochondrial autophagy. Through IKK-NF-κB-COX-2, SHP-2-MEK-1-ERK, and SHP-2-Ras-ERK anti-angiogenic pathways, ConA would inhibit cancer cell survival. In addition, ConA stimulates cell immunity and generates an immune memory, resisting to the same genotypic tumor. These biological findings shed light on new perspectives of ConA as a potential anti-neoplastic agent targeting apoptosis, autophagy and anti-angiogenesis in pre-clinical or clinical trials for cancer therapeutics.
刀豆球蛋白 A（ConA）是一种 Ca(2+)/Mn(2+)依赖性、甘露糖/葡萄糖结合的豆科植物凝集素，由于其对多种癌细胞具有显著的抗增殖和抗肿瘤活性而受到越来越多的关注。ConA 通过线粒体介导的、P73-Foxo1a-Bim 凋亡和 BNIP3 介导的线粒体自噬诱导程序性细胞死亡。通过 IKK-NF-κB-COX-2、SHP-2-MEK-1-ERK 和 SHP-2-Ras-ERK 抗血管生成途径，ConA 抑制癌细胞存活。此外，ConA 刺激细胞免疫并产生免疫记忆，抵抗同种基因型的肿瘤。这些生物学发现为 ConA 作为一种潜在的抗肿瘤药物提供了新的视角，该药物可针对凋亡、自噬和抗血管生成在临床前或临床试验中用于癌症治疗。
