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Inhibition of nuclear factor-κB activity enhanced chemosensitivity to cisplatin in human lung adeno-carcinoma A549 cells under chemical hypoxia conditions

Li, Fang ; Huang, Li ; Su, Xiao-Li ; Gu, Qi-Hua ; Hu, Cheng-Ping

Chinese medical journal, 2013, Vol.126 (17), p.3276-3282 [Periódico revisado por pares]

China: Department of Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, Hunan 410007, China

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  • Título:
    Inhibition of nuclear factor-κB activity enhanced chemosensitivity to cisplatin in human lung adeno-carcinoma A549 cells under chemical hypoxia conditions
  • Autor: Li, Fang ; Huang, Li ; Su, Xiao-Li ; Gu, Qi-Hua ; Hu, Cheng-Ping
  • Assuntos: A549细胞 ; Adenocarcinoma - metabolism ; Adenocarcinoma of Lung ; Apoptosis - drug effects ; Cell Line, Tumor ; Cell Survival - drug effects ; Cisplatin - pharmacology ; Humans ; Hypoxia - physiopathology ; Lung Neoplasms - metabolism ; NF-kappa B - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Western印迹法 ; 化学性 ; 核因子-κB ; 缺氧条件 ; 缺氧诱导因子-1 ; 肺腺癌 ; 顺铂
  • É parte de: Chinese medical journal, 2013, Vol.126 (17), p.3276-3282
  • Notas: Background Tumor hypoxia, one of the features of solid tumors, is associated with chemo-resistance. Recently, nuclear factor-KB （NF-κB） was found to be activated during hypoxia. However, the impact of NF-κB activation on chemo-resistance during hypoxia remains unknown. Methods Human lung adenocarcinoma A549 cells were transfected with NF-κB p65siRNA and treated with cobalt chloride （COCI2） to mimic hypoxia in the presence or absence of cisplatin. NF-KB expression was measured by Western blotting, immune-fluorescence and real-time PCR. Hypoxia-inducible factor-1α （HIF-1α） and Bcl-2 expression were determined by Western blotting. Cell apoptosis and survival with half-maximum inhibitory concentration （IC50） of cisplatin were determined by Annexin V-FITC/PI and 3-（4, 5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT）, respectively. Results Exposure ofA549 cells to COCl2 increased nuclear HIF-1α protein expression, and enhanced NF-KB p65 protein nuclear accumulation （the mark of NF-κB activation） in a time and dose dependant manner. COCI2 did not promote apoptosis in A549 cells; on the contrary, it reduced cisplatin-induced apoptosis and increased the IC50 of cisplatin. However, when we inhibited CoCI2-induced activation of NF-κB through NF-κB p65siRNA, cisplatin-induced apoptosis was increased and IC50 of cisplatin was reduced to levels similar to those in control cells. Meanwhile, CoCI2-induced Bcl-2 over- expression was down-regulated in the presence of cisplatin when NF-κB activity was inhibited. Conclusion Up-regulating Bcl-2 might be involved in NF-κB activation induced resistance to cisplatin in A549 cells under CoCl2-induced chemical hypoxia.
    11-2154/R
    lung adenocarcinoma; nuclear factor-κB; chemical hypoxia; chemotherapy; Bcl-2
    ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Background Tumor hypoxia, one of the features of solid tumors, is associated with chemo-resistance. Recently, nuclear factor-KB （NF-κB） was found to be activated during hypoxia. However, the impact of NF-κB activation on chemo-resistance during hypoxia remains unknown. Methods Human lung adenocarcinoma A549 cells were transfected with NF-κB p65siRNA and treated with cobalt chloride （COCI2） to mimic hypoxia in the presence or absence of cisplatin. NF-KB expression was measured by Western blotting, immune-fluorescence and real-time PCR. Hypoxia-inducible factor-1α （HIF-1α） and Bcl-2 expression were determined by Western blotting. Cell apoptosis and survival with half-maximum inhibitory concentration （IC50） of cisplatin were determined by Annexin V-FITC/PI and 3-（4, 5-dimethylthiazol-2-yl）-2, 5-diphenyltetrazolium bromide （MTT）, respectively. Results Exposure ofA549 cells to COCl2 increased nuclear HIF-1α protein expression, and enhanced NF-KB p65 protein nuclear accumulation （the mark of NF-κB activation） in a time and dose dependant manner. COCI2 did not promote apoptosis in A549 cells; on the contrary, it reduced cisplatin-induced apoptosis and increased the IC50 of cisplatin. However, when we inhibited CoCI2-induced activation of NF-κB through NF-κB p65siRNA, cisplatin-induced apoptosis was increased and IC50 of cisplatin was reduced to levels similar to those in control cells. Meanwhile, CoCI2-induced Bcl-2 over- expression was down-regulated in the presence of cisplatin when NF-κB activity was inhibited. Conclusion Up-regulating Bcl-2 might be involved in NF-κB activation induced resistance to cisplatin in A549 cells under CoCl2-induced chemical hypoxia.
  • Editor: China: Department of Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, Hunan 410007, China
  • Idioma: Inglês
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