Phyllanthus taxodiifolius Beille Disrupted N-cadherin, Vimentin, Paxillin and Actin Stress Fibers in Glioblastoma
Issued Date
2022-01-01
Resource Type
ISSN
15137368
eISSN
2476762X
Scopus ID
2-s2.0-85135257141
Pubmed ID
35901345
Journal Title
Asian Pacific Journal of Cancer Prevention
Volume
23
Issue
7
Start Page
2379
End Page
2386
Rights Holder(s)
SCOPUS
Bibliographic Citation
Asian Pacific Journal of Cancer Prevention Vol.23 No.7 (2022) , 2379-2386
Suggested Citation
Sunrat C., Kwanthongdee J., Uppakara K., Chabang N., Munyoo B., Tuchinda P., Saengsawang W. Phyllanthus taxodiifolius Beille Disrupted N-cadherin, Vimentin, Paxillin and Actin Stress Fibers in Glioblastoma. Asian Pacific Journal of Cancer Prevention Vol.23 No.7 (2022) , 2379-2386. 2386. doi:10.31557/APJCP.2022.23.7.2379 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/83890
Title
Phyllanthus taxodiifolius Beille Disrupted N-cadherin, Vimentin, Paxillin and Actin Stress Fibers in Glioblastoma
Other Contributor(s)
Abstract
Objective: Glioblastoma is the most aggressive and lethal brain tumor in adults with highly invasive properties. In this present study, we explored the effects of Phyllanthus taxodiifolius Beille extract on molecules known to be hallmarks of aggressive glioblastoma including N-cadherin and vimentin, mesenchymal markers, as well as paxillin, a major adaptor protein that regulates the linking of focal adhesions to the actin cytoskeleton. Methods: P. taxodiifolius were air-dried, powdered and percolated with methanol, filtered, concentrated and lyophilized to yield a crude methanol extract. C6 glioblastoma cell line was used in this study. The expression of N-cadherin and vimentin, as well as the activation of paxillin was determined using Western blot analysis. The effect of the extract on focal adhesions and actin cytoskeleton were investigated using immunofluorescence staining and confocal imaging. Results: In the presence of 40 μg/ml Phyllanthus taxodiifolius Beille extract, the expression of N-cadherin and vimentin were significantly decreased (p<0.001 and p<0.05, respectively). Activation of paxillin was also diminished as indicated by a reduction of phosphorylated-paxillin (p<0.01). Consequently, actin stress fibers in glioblastoma cells were abolished as evidenced by the decrease in focal adhesion (p<0.001) and stress fibers numbers (p<0.001). Conclusion: Our study demonstrates for the first time that P. taxodiifolius interferes with multiple key molecules related to pathological hallmarks of glioblastoma. These molecules are involved with cell contacts, focal adhesions, and the formation and stabilization of actin stress fibers, which are required for glioblastoma metastatic behavior. These results provide further evidence supporting the potential of P. taxodiifolius and its bioactive compounds as anti-cancer agents.