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AKT1 and AKT2 promote malignant transformation in human brain glioma LN229 cells

  • Published:
Clinical Oncology and Cancer Research

Abstract

Objective

To confirm the role played by AKT1 and AKT2 in the β-catenin/ Tcf-4 signaling pathway in promoting malignant transformation of glioma cells.

Methods

LN229 cells were divided into five groups: a control group, acetone (ACE)group, acetylsalicylic acid (ASA; aspirin) group, ASA+AKT1 plasmid group and ASA+AKT2 plasmid group. Western blot and PCR were used to detect the expression of AKT1 and AKT2 after dealing with ASA and transferring AKT1/2 genes into LN229 cells. Cell proliferation was determined by flow cytometry, cell invasion was evaluated by transwell assay and cell apoptosis was detected with annexin V staining. The molecules regulating proliferation and invasion were examined by western blot analysis.

Results

Aspirin down-regulates AKT1 and AKT2 expression by modulating b-catenin/Tcf-4 activity. AKT1 and AKT2 can enhance cell proliferation and invasion by up-regulating the expression of cyclin-D and matrix metalloprotein-9 (MMP-9) in LN229 glioma cells.

Conclusion

AKT1 and AKT2 play an important role in the bcatenin/Tcf-4 signaling pathway promoting malignant transformation; AKT1 is more effective than AKT2. AKT1 and AKT2 may be potential targets for brain glioma therapy and an effective way to prevent metastasis of gliomas.

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Authors and Affiliations

  1. Department of Neurosurgery, Tianjin Medical University General Hospital, Laboratory of Neuro-oncology, Tianjin Neurological Institute, Tianjin, 300052, China

    Jian Zou, Kun Wang, Lei Han, An-ling Zhang, Zhen-dong Shi, Pei-yu Pu & Chun-sheng Kang

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  1. Jian Zou
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  2. Kun Wang
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  4. An-ling Zhang
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  7. Chun-sheng Kang
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Corresponding author

Correspondence to Chun-sheng Kang.

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Cite this article

Zou, J., Wang, K., Han, L. et al. AKT1 and AKT2 promote malignant transformation in human brain glioma LN229 cells. Clin. Oncol. Cancer Res. 8, 144–148 (2011). https://doi.org/10.1007/s11805-011-0573-9

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  • DOI: https://doi.org/10.1007/s11805-011-0573-9

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