Inhibitions and mechanisms of amygdalin in non-small cell lung cancer NCI-H1299 cell line invasion<i> in vitro</i>

SUN Zhuolin; LIU Jingwei; KUANG Changchun

doi:10.11665/j.issn.1000-5048.20160415

Journal of China Pharmaceutical University > 2016 > 47(4): 479-482. > DOI: 10.11665/j.issn.1000-5048.20160415

SUN Zhuolin, LIU Jingwei, KUANG Changchun. Inhibitions and mechanisms of amygdalin in non-small cell lung cancer NCI-H1299 cell line invasion in vitro[J]. Journal of China Pharmaceutical University, 2016, 47(4): 479-482. DOI: 10.11665/j.issn.1000-5048.20160415

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Inhibitions and mechanisms of amygdalin in non-small cell lung cancer NCI-H1299 cell line invasion in vitro

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The aim of this study was to investigate the effects and mechanisms of a nature product, amygdalin, in non-small cell lung cancer NCI-H1299 cell line invasion and migration in vitro. NCI-H1299(H1299)cells were treated with amygdalin. MTS assay was employed to determine cell proliferation, transwell chamber and wound-healing assay were employed to determine invasion and migration in vitro, western blotting and RT-PCR assay were employed to determine the expression of integrin β1, integrin β4, integrin-linked kinase(ILK), focal adhesion kinase(FAK), p-FAK and β-catenin, and the phosphorylation of Akt and RICTOR. Results showed that in vitro proliferation of H1299 cells were inhibited significantly after treated with 0. 5 and 1 mg/mL amygdalin for 48 h. The invasion and migration potential was decreased. The protein and mRNA expression of MMP-2/9, integrin β1/4, ILK, FAK, β-catenin, the activity of MMP-2/9, the phosphorylation of FAK, Akt and RICTOR were all decreased significantly(all of P< 0. 05).
- amygdalin,
- non-small cell lung cancer,
- metastasis,
- NCI-H1299,
- integrin-linked kinase,
- focal adhesion kinase

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Inhibitions and mechanisms of amygdalin in non-small cell lung cancer NCI-H1299 cell line invasion in vitro

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