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Effect of NF-κB inhibitors on the chemotherapy-induced apoptosis of the colon cancer cell line HT-29

This study aimed to investigate the impact of the combined use of the nuclear factor-κB (NF-κB) inhibitors pyrrolidine dithiocarbamate (PDTC), bortezomib or SN50, and the chemotherapy agents arsenic acid (As(2)O(3)), fluorouracil (5FU), oxaliplatin or paclitaxel on the growth and apoptosis of HT-29...

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Detalles Bibliográficos
Autores principales: LIU, TING, LIU, DAN, LIU, JING, SONG, JI-TAO, GAO, SHAN-LING, LI, HUI, HU, LI-HONG, LIU, BING-RONG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501445/
https://www.ncbi.nlm.nih.gov/pubmed/23170132
http://dx.doi.org/10.3892/etm.2012.647
Descripción
Sumario:This study aimed to investigate the impact of the combined use of the nuclear factor-κB (NF-κB) inhibitors pyrrolidine dithiocarbamate (PDTC), bortezomib or SN50, and the chemotherapy agents arsenic acid (As(2)O(3)), fluorouracil (5FU), oxaliplatin or paclitaxel on the growth and apoptosis of HT-29 cells. Cell morphology was observed using inverted microscopy, and cell viability and apoptosis were assessed using the MTT assay and flow cytometry, respectively. The activities of NF-κB were analyzed by western blotting and electrophoretic mobility shift assay (EMSA). Cell growth was significantly inhibited by As(2)O(3), oxaliplatin and paclitaxel in a time- and concentration-dependent manner (P<0.05), while 5FU inhibited cell growth in a time-dependent manner only (P<0.05). The growth inhibition rate and apoptosis induction ratio were increased following the combined treatment of the chemotherapy agent and NF-κB inhibitor. The expression of NF-κB p65 was upregulated when cells were treated with a chemotherapy drug, however it was downregulated following combined treatment or treatment with an NF-κB inhibitor alone. In conclusion, an NF-κB inhibitor combined with a chemotherapy drug effectively inhibited cell proliferation, induced cell apoptosis and inhibited NF-κB activity to enhance the chemotherapeutic sensitivity of HT-29 cells.