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Targeting GRP78 as a Basis for Enhanced Glioma Cells Killing by Anti-TfR Antibody
Xue Wen1, Xiaoping Cheng, Si Wu
1Hubei Polytechnic Institute, School of Nursing, Department of Basic Medical, Xiaogan, China.
Aim:
Studies have illustrated that chemotherapeutic drugs induce endoplasmic reticulum (ER) stress in glioblastoma cells. In our previous studies, it is clear that anti-transferrin receptor (anti-TfR) monoclonal antibody (mAB) 7579 enhanced anti-tumor effects of chemotherapeutic drugs on human glioma cells in vitro. In our study, we therefore investigated how the anti-TfR antibody increased ER stress, alone or in combination with a chemotherapeutic drug.
Material And Methods:
ER stress was detected after cells were treated with anti-TfR mAb and/or Nimustine by western blot analysis. The colony survival and apoptosis of cells were detected after transfection with small interfering RNA (siRNA) and treatment with anti-TfR mAb and/or Nimustine by labeling with methylene blue and FCM.
Results:
The anti-TfR antibody combined with Nimustine could elevate expression of GRP78/BiP and CHOP/GADD153 and further increase ER stress. SiRNA against the ER stress marker GRP78 produced a further sensitization of glioma cells to killing by the anti-TfR antibody and/or Nimustine.
Conclusion:
Our results show the anti-TfR antibody triggers the ER stress response. Furthermore, this anti-tumor effect is achieved via the siRNA against GRP78 for glioma cell growth and its survival. These results hold promise as a clinical approach to gene therapy for malignant gliomas.
