HE Lan, ZHOU Fang-Liang, ZOU Pan, WANG Xian-Wen, JIANG Yi-Lan, HE Ying-Chun, LIAO Duan-Fang, CAO De-Liang. Yi Qi Jie Du Formula and Salinomycin Combination Treatment Mediates Nasopharyngeal Carcinoma Stem Cell Proliferation, Migration and Apoptosis via CD44/Ras Signaling Pathway[J]. Digital Chinese Medicine, 2020, 3(4): 297-308. DOI: 10.1016/j.dcmed.2020.12.008
Citation: HE Lan, ZHOU Fang-Liang, ZOU Pan, WANG Xian-Wen, JIANG Yi-Lan, HE Ying-Chun, LIAO Duan-Fang, CAO De-Liang. Yi Qi Jie Du Formula and Salinomycin Combination Treatment Mediates Nasopharyngeal Carcinoma Stem Cell Proliferation, Migration and Apoptosis via CD44/Ras Signaling Pathway[J]. Digital Chinese Medicine, 2020, 3(4): 297-308. DOI: 10.1016/j.dcmed.2020.12.008

Yi Qi Jie Du Formula and Salinomycin Combination Treatment Mediates Nasopharyngeal Carcinoma Stem Cell Proliferation, Migration and Apoptosis via CD44/Ras Signaling Pathway

  • ObjectiveTo assess the effects of Yi Qi Jie Du Formula (YQJDF) combined with salinomycin (SAL) on nasopharyngeal carcinoma stem cells (NPC-SCs) and investigate the underlying molecular mechanisms.
    MethodsCell counting methods, the CCK-8 assay, transwell migration assay and JC-1 staining, were used to observe the effects of the combination on the proliferation, migration and apoptosis of NPC stem cells, respectively. Western blot was used to detect the levels of protein in NPC-SCs.
    ResultsYQJDF combined with SAL had a synergistic effect on the inhibition of proliferation and migration and induction of NPC-SC apoptosis. Mechanistically, YQJDF combined with SAL synergistically upregulated the levels of apoptotic proteins, including cleaved Caspase-3, cleaved Caspase-7 and cleaved Caspase-9. Moreover, YQJDF combined with SAL synergistically decreased the levels of CD44, p-c-Src, Ras, p-PKCδ, p-MEK, p-c-Raf, p-ERK1/2 and p-AKT proteins.
    ConclusionsThe combination of YQJDF and SAL has a synergistic effect on the inhibition of NPC-SC proliferation and migration and induction of apoptosis, which may be closely related to the downregulation of the CD44/Ras signaling pathway.
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