Molecular mechanisms of Lycoris aurea agglutinin-induced apoptosis and G2/M cell cycle arrest in human lung adenocarcinoma A549 cells, both in vitro and in vivo

Objectives Lycoris is aurea agglutinin (LAA) has attracted rising attention due to its remarkable bioactivities. Here, we aimed at investigating its anti‐tumor activities. Material and Methods In vitro methods including MTT, cellular morphology observation, FCM and immunoblotting were performed. In...

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Veröffentlicht in:Cell proliferation 2013-06, Vol.46 (3), p.272-282
Hauptverfasser: Li, C.-Y., Wang, Y., Wang, H.-L., Shi, Z., An, N., Liu, Y.-X., Liu, Y., Zhang, J., Bao, J.-K., Deng, S.-P.
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Sprache:eng
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Zusammenfassung:Objectives Lycoris is aurea agglutinin (LAA) has attracted rising attention due to its remarkable bioactivities. Here, we aimed at investigating its anti‐tumor activities. Material and Methods In vitro methods including MTT, cellular morphology observation, FCM and immunoblotting were performed. In vivo methods like detection of tumor volume, body weight and survival ratio, as well as TUNEL staining were performed. Results and Conclusion LAA triggers G2/M phase cell cycle arrest via up‐regulating p21expression as well as down‐regulating cdk‐1cyclinA singling pathway, and induces apoptotic cell death through inhibiting PI3K‐Akt survival pathway in human lung adenocarcinoma A549 cells. While LAA has no significant cytotoxic effect toward normal human embryonic lung fibroblast HELF cells, and moreover, LAA could amplify the antineoplastic effects of cisplatin toward A549 cells. Lastly LAA also bears anti‐cancer and apoptosis‐inducing effects in vivo, and it could decrease the volume and weight of subcutaneous tumor mass obviously as well as expand lifespan of mice. These findings may provide a new perspective for elucidating the complicated molecular mechanisms of LAA‐induced cancer cell growth‐inhibition and death, providing a new opportunity of LAA as a potential candidate anti‐neoplastic drug for future cancer therapeutics.
ISSN:0960-7722
1365-2184
DOI:10.1111/cpr.12034