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Proteomic analysis of apoptosis induction in human lung cancer cells by recombinant MVL
Yuqin Li1, Bochao Zhang, Xiaoqin Wang
1College of Light Industry and Food Sciences, South China University of Technology, 381 Wushan Road, Guangzhou, 510640, China.
Abstract:
Lung cancer is still difficult to treat by current chemotherapeutic procedures. We recently found that MVL, an anti-HIV lectin from blue-green algae Microcystis viridis, also has antitumor activity. The objective of this study was to investigate apoptosis-inducing activity of recombinant MVL (R-MVL) and proteomic changes in A549 cells, and to identify the molecular pathways responsible for the anti-cancer action of R-MVL. We found that R-MVL induces A549 cells apoptosis in a dose-dependent manner by using MTT assay, fluorescent microscope (FM) and flow cytometry (FCM), and the IC50 was calculated to be 24.12 μg/ml. Subsequently, 7 altered proteins in R-MVL-treated A549 cells were identified, including upregulated aldehyde dehydrogenase 1 and β-actin, and five downregulated proteins: heat shock protein 90, heat shock 60, plastin 3, tropomyosin 3, and β-tubulin. Further bioinformatics analysis predicted the potential pathways for R-MVL to induce apoptosis of A549 cells. In conclusion, this is the first report to investigate anti-cancer activity of R-MVL and its mechanism of action by proteomics analysis. Our observations provide potential therapeutic targets for lung cancer inhibitor intervention and implicated the development of novel anti-cancer therapeutic strategies.
Insights
Recombinant Microcystis viridis lectin (R-MVL) shows potent anti-lung cancer activity by inducing apoptosis in A549 cells. Proteomic analysis identified key protein changes, revealing potential therapeutic targets for novel lung cancer treatments.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Research
Background:
- Lung cancer remains challenging to treat with conventional chemotherapy.
- Microcystis viridis lectin (MVL), an anti-HIV lectin, exhibits potential antitumor properties.
Purpose of the Study:
- To investigate the apoptosis-inducing effects of recombinant MVL (R-MVL) on A549 lung cancer cells.
- To identify proteomic alterations and molecular pathways involved in R-MVL's anti-cancer mechanism.
Main Methods:
- MTT assay, fluorescence microscopy (FM), and flow cytometry (FCM) were used to assess apoptosis and determine IC50.
- Proteomic analysis identified differentially expressed proteins in R-MVL-treated A549 cells.
- Bioinformatics tools were employed to predict molecular pathways.
Main Results:
- R-MVL induced apoptosis in A549 cells in a dose-dependent manner, with an IC50 of 24.12 μg/ml.
- Seven proteins were altered, including upregulated aldehyde dehydrogenase 1 and β-actin, and downregulated heat shock proteins (HSP90, HSP60), plastin 3, tropomyosin 3, and β-tubulin.
- Bioinformatics analysis suggested potential apoptosis-related pathways targeted by R-MVL.
Conclusions:
- This study is the first to demonstrate the anti-cancer activity of R-MVL against lung cancer using proteomics.
- R-MVL exhibits significant apoptosis-inducing effects on A549 cells.
- The identified protein changes and pathways offer potential therapeutic targets for novel lung cancer interventions.
