Cariporide sensitizes leukemic cells to tumor necrosis factor related apoptosis-inducing ligand by up-regulation of death receptor 5 via endoplasmic reticulum stress-CCAAT/enhancer binding protein homologous protein dependent mechanism.

@article{Li2014CariporideSL,
  title={Cariporide sensitizes leukemic cells to tumor necrosis factor related apoptosis-inducing ligand by up-regulation of death receptor 5 via endoplasmic reticulum stress-CCAAT/enhancer binding protein homologous protein dependent mechanism.},
  author={Huawen Li and Guoqiang Chang and Jian You Wang and Lihong Wang and Weina Jin and Yani Lin and Yan Yan and Ruojun Wang and Wei Gao and Li Ma and Qinghua Li and Tianxiang Pang},
  journal={Leukemia & lymphoma},
  year={2014},
  volume={55 9},
  pages={
          2135-40
        }
}
CCAAT/enhancer binding protein homologous protein (CHOP) expression increases when Na(+)-H(+) exchanger 1 (NHE1) is inhibited. Endoplasmic reticulum (ER) stress has been shown to trigger tumor cell death through CHOP. We therefore hypothesized that NHE1 activity correlates with ER stress and confers pharmaceutical potential to NHE1 inhibitor as an anti-tumor agent. The present study showed that treatment with the NHE1 inhibitor cariporide led to ER stress-induced up-regulation of the death… CONTINUE READING
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