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Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-960917

RESUMO

ObjectiveTo investigate effect of astragaloside Ⅳ on the proliferation, migration, and invasion of colorectal cancer HCT116 cells and the underlying molecular mechanism. MethodColorectal cancer HCT116 cells were classified into blank group (DMSO) and low-dose (15.7 mg·L-1), medium-dose (31.4 mg·L-1), and high-dose (62.8 mg·L-1) astragaloside Ⅳ groups. After drug treatment, the morphological changes of HCT116 cells were observed under an inverted microscope. Cell viability was detected by cell counting kit-8 (CCK-8) assay, and the migration and invasion of cells were detected based on scratch assay and Transwell assay. The expression of cyclin-dependent kinase inhibitor (p21), CyclinD1, B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax) in the cells was examined by Western blot. ResultCompared with the blank group, cells in the three astragaloside Ⅳ groups demonstrated slow growth, low density, inconsistent morphology, nuclear shrinkage, degradation of cytoplasm, and high death rate. Moreover, cell viability decreased in a concentration-dependent manner in the astragaloside Ⅳ groups. Cell migration and invasion were inhibited (P<0.05, P<0.01), and the inhibition rate was in positive correlation with the concentration of the astragaloside Ⅳ. The expression of pro-apoptotic protein Bax in low-dose, medium-dose and high-dose astragaloside Ⅳ groups increased gradually in a concentration-dependent manner, while the expression of p21, CyclinD1 and anti-apoptotic protein Bcl-2 decreased gradually in a concentration-dependent manner compared with those in the blank group (P<0.05, P<0.01). ConclusionAstragaloside Ⅳ can suppress the proliferation, migration, and invasion of colorectal cancer HCT116 cells and promote the apoptosis, thus inhibiting the occurrence and development of colorectal cancer.

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