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Downregulation of galectin-3 by EGF mediates the apoptosis of HepG2 cells

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Abstract

Epidermal growth factor (EGF) in high concentrations induces apoptosis of the tumor cells which express high levels of epidermal growth factor receptor. However, the precise mechanism for this induction is not clear. Galectin-3 is the most probable candidate for mediating this effect, as it is known to induce anti-apoptotic activity in a variety of tumor cells exposed to diverse apoptotic stimuli. In this study, we determined whether galectin-3 plays a role in high concentrations of EGF-induced apoptosis of HepG2 cells. We found that EGF in high concentrations led to the growth inhibition of HepG2 cells, which were associated with promotion of cell death. High concentrations of EGF suppressed cytoplasmic expression of galectin-3. Moreover, we demonstrated overexpression of galectin-3 could reduce EGF-induced apoptosis in HepG2 cells. Our study demonstrated for the first time that downregulation of cytoplasmic galectin-3 was essential for high concentrations of EGF-induced apoptosis in HepG2 cells.

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Abbreviations

EGF:

Epidermal growth factor

EGFR:

Epidermal growth factor receptor

Raf1:

V-raf-1 murine leukemia viral oncogene homolog 1

PI3K:

Phosphatidylinositol 3-kinase

AKT:

Protein kinase B

ERK:

Extracellular signal-regulated protein kinase

GFP:

Green fluorescent protein

STAT1:

Signal transducer and activator of transcription 1

BCL-2:

B cell lymphoma 2

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Acknowledgments

We thank Dr. Zhiwei Wu and Dr. Hong Wang for their critical reading. The work was supported by grants from the Health Department of Jiangsu (No. H200824), the Program for Advanced Talents within Six Industries of Jiangsu (07-B-023), and the Research Program funded by Nanjing Medical University (2005NYD2D17) to DT.

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Correspondence to Datong Zheng.

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Hu, Z., Jiang, X., Xu, Y. et al. Downregulation of galectin-3 by EGF mediates the apoptosis of HepG2 cells. Mol Cell Biochem 369, 157–165 (2012). https://doi.org/10.1007/s11010-012-1378-8

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  • DOI: https://doi.org/10.1007/s11010-012-1378-8

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