Abstract
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.
Copyright © 2011 Elsevier Inc. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amino Acid Sequence
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Angiogenesis Inhibitors / chemistry
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Angiogenesis Inhibitors / pharmacology*
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Angiogenesis Inhibitors / therapeutic use
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Antineoplastic Agents / chemistry
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents / therapeutic use
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Apoptosis / drug effects*
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Autophagy / drug effects*
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Cell Survival / drug effects
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Concanavalin A / chemistry
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Concanavalin A / pharmacology*
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Concanavalin A / therapeutic use
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Humans
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MAP Kinase Signaling System
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Molecular Sequence Data
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Neoplasms / blood supply
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Neoplasms / drug therapy*
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Neoplasms / enzymology
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Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism
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ras Proteins / metabolism
Substances
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Angiogenesis Inhibitors
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Antineoplastic Agents
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Concanavalin A
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PTPN11 protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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ras Proteins