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Endoplasmic reticulum stress ( ERS ) plays an important role in the pathogenesis and development of malignant tumors, as well as in the regulation of radiochemoresistance and chemoresistance in many malignancies.  ERS  signaling pathway protein kinase  RNA ‐like endoplasmic reticulum kinase ( PERK )‐eukaryotic initiation factor‐2 ( eIF 2α) may induce aberrant activation of nuclear factor‐κB ( NF ‐κB). Our previous study showed that  NF ‐κB conferred radioresistance in lymphoma cells. However, whether  PERK ‐ eIF 2α regulates radioresistance in oropharyngeal carcinoma through  NF ‐κB activation is unknown. Herein, we showed that  PERK  overexpression correlated with a poor prognosis for patients with oropharyngeal carcinoma ( P  < 0.01). Meanwhile, the percentage of the high expression level of  PERK  in oropharyngeal carcinoma patients resistant to radiation was higher than in patients sensitive to radiation (77.7 and 33.3%, respectively;  P  < 0.05). Silencing  PERK  and  eIF 2α increased the radiosensitivity in oropharyngeal carcinoma cells and increased radiation‐induced apoptosis and G2/M phase arrest.  PERK ‐ eIF 2α silencing also inhibited radiation‐induced  NF ‐κB phosphorylation and increased the  DNA  double strand break‐related proteins  ATM  phosphorylation.  NF ‐κB activator  TNF ‐α and the  ATM  inhibitor Ku55933 offset the regulatory effect of  eIF 2α on the expression of radiation‐induced cell apoptosis‐related proteins and the G2/M phase arrest‐related proteins. These data indicate that  PERK  regulates radioresistance in oropharyngeal carcinoma through  NF ‐ kB  activation‐mediated phosphorylation of  eIF 2α, enhancing X‐ray‐induced activation of  DNA DSB  repair, cell apoptosis inhibition and G2/M cell cycle arrest.

Endoplasmic reticulum stress pathway PERK ‐ eIF 2α confers radioresistance in oropharyngeal carcinoma by activating NF ‐κB