A Novel Molecular Model of Plant Lectin-Induced Programmed Cell Death in Cancer

Biol Pharm Bull. 2017 Oct 1;40(10):1625-1629. doi: 10.1248/bpb.b17-00363. Epub 2017 Aug 1.

Abstract

Plant lectin, a class of highly diverse non-immune origin and carbohydrate-binding proteins, has been reported to specially induce cancer cell through programmed cell death (PCD) pathways (apoptosis and/or autophagy), shedding lights on screening promising anti-cancer candidate agent for further therapeutic trials. However, the complicated molecular mechanisms by which plant lectins induced the programmed death of tumor cells, have not yet been fully clarified. Here, we summarized a novel model, based on vast amount of research, by which plant lectins eliminate various types of cancer cells via three major pathways, including a) direct ribosome inactivating, b) endocytosis-dependent mitochondrial dysfunction and c) sugar-containing receptors binding. A better understanding of the role of plant lectins played and further elucidation of the strategies targeting PCD would provide a new clue for the applications and modifications of plant lectin as a potential anti-cancer agent from bench to clinic.

Keywords: apoptosis; autophagy; drug development; molecular model; plant lectin; programmed cell death.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / chemistry
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Autophagy / drug effects*
  • Concanavalin A / pharmacology
  • HT29 Cells
  • Humans
  • Jurkat Cells
  • Models, Molecular
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Plant Lectins / chemistry
  • Plant Lectins / pharmacology*
  • Signal Transduction / drug effects

Substances

  • Antineoplastic Agents
  • Plant Lectins
  • Concanavalin A