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Published on: February 6, 2015
In silico and experimental studies of concanavalin A: insights into its antiproliferative activity and apoptotic
Zhongyu Liu1, Xufeng Li, Xianping Ding
1College of Life Sciences, Sichuan University, Chengdu 610064, China. zhongyujohn@gmail.com
Abstract:
Concanavalin A (ConA), a mannose/glucose-binding legume lectin, has been reported to induce tumor cell death via a mitochondria-mediated autophagic pathway; however, the precise mechanism by which induces cell death remains to be discovered. In this study, we simulated the three-dimensional structure of ConA monomer, its dimer, and tetramer forms and reported its molecular dynamics simulations and phylogenetic analysis. Subsequently, we showed that ConA possessed remarkable antiproliferative effects on HepG2 cells. Further data showed that there was a link among its hemagglutinating, sugar-binding, and antiproliferative activities. In addition, we found that ConA induced apoptosis in HepG2 cells. Then, we demonstrated that the treatment of ConA caused mitochondrial transmembrane potential (MMP) collapse, cytochrome c release, and activation of caspase. In conclusion, we demonstrate that there is a positive correlation between carbohydrate-binding activity and antiproliferative activity of ConA. In addition, we confirm that ConA induces HepG2 cell death through a mitochondrial apoptotic pathway.
Insights
Concanavalin A (ConA) exhibits significant antiproliferative effects on HepG2 cells. This lectin induces cancer cell death through a mitochondrial apoptotic pathway, correlating with its carbohydrate-binding activity.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- Concanavalin A (ConA), a lectin, is known to induce tumor cell death.
- The precise mechanism of ConA-induced cell death, particularly its apoptotic pathway, requires further elucidation.
Purpose of the Study:
- To investigate the mechanism of ConA-induced cell death in HepG2 cells.
- To explore the correlation between ConA's structural properties, binding activities, and antiproliferative effects.
Main Methods:
- 3D structural simulation and molecular dynamics of ConA forms (monomer, dimer, tetramer).
- Phylogenetic analysis of ConA.
- Assessment of ConA's antiproliferative effects on HepG2 cells.
- Analysis of apoptosis markers: mitochondrial transmembrane potential (MMP), cytochrome c release, and caspase activation.
Main Results:
- ConA demonstrated significant antiproliferative effects on HepG2 cells.
- A direct link was established between ConA's hemagglutinating, sugar-binding, and antiproliferative activities.
- ConA induced apoptosis in HepG2 cells via mitochondrial pathway, evidenced by MMP collapse, cytochrome c release, and caspase activation.
Conclusions:
- ConA induces HepG2 cell death through a mitochondrial apoptotic pathway.
- A positive correlation exists between the carbohydrate-binding activity and the antiproliferative activity of ConA.
