Concanavalin A (ConA), the most studied plant lectin, has been known as a potent anti-neoplastic agent for a long time. Since initial reports on its capacity to kill cancer cells, much attention has been devoted to unveiling the lectin's exact molecular mechanism. It has been revealed that ConA can bind to several receptors on cancerous and normal cells and modulate the related signaling cascades. The most studied host receptor for ConA is MT1-MMP, responsible for most of the lectin's modulations, ranging from activating immune cells to killing tumor cells. In this study, in addition to studying the effect of ConA on signaling and immune cell function, we will focus on the most up-to-date advancements that unraveled the molecular mechanisms by which ConA can induce autophagy and apoptosis in various cancer cell types, where it has been found that P73 and JAK/STAT3 are the leading players. Moreover, we further discuss the main signaling molecules causing liver injury as the most significant side effect of the lectin injection. Altogether, these findings may shed light on the complex signaling pathways controlling the diverse responses created via ConA treatment, thereby modulating these complex networks to create more potent lectin-based cancer therapy.

中文翻译：

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刀豆球蛋白 A 作为一种有前途的基于凝集素的抗癌剂：分子机制和治疗潜力

刀豆球蛋白 A (ConA) 是研究最多的植物凝集素，长期以来一直被认为是一种有效的抗肿瘤药物。自从关于其杀死癌细胞的能力的初步报道以来，很多注意力都集中在揭示凝集素的确切分子机制上。据透露，ConA 可以与癌细胞和正常细胞上的几种受体结合，并调节相关的信号级联反应。研究最多的 ConA 宿主受体是 MT1-MMP，负责大多数凝集素的调节，范围从激活免疫细胞到杀死肿瘤细胞。在这项研究中，除了研究 ConA 对信号传导和免疫细胞功能的影响外，我们还将关注最新进展，这些进展揭示了 ConA 可以在各种癌细胞类型中诱导自噬和凋亡的分子机制，其中发现 P73 和 JAK/STAT3 是主要参与者。此外，我们进一步讨论了导致肝损伤的主要信号分子是凝集素注射最显着的副作用。总而言之，这些发现可能会阐明控制通过 ConA 治疗产生的不同反应的复杂信号通路，从而调节这些复杂的网络以产生更有效的基于凝集素的癌症治疗。