Characterization and Expression Analysis of Peroxiredoxin Genes in NNK-induced V79 Cells

Considering that lung cancer is largely caused by tobacco smoke carcinogens such as NNK and that the majority of all lung cancer tumor tissue extracts express high levels of Prxs, our study investigates the association between these two molecules

ZHOU Wen Shan; HAN Ya Wei; SHI Gui Qin

2017

Scholarcy highlights

  • 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone is a potent and prevalent nitrosamine procarcinogen found in cigarette smoke
  • Besides exerting a direct oxidant effect, cigarette smoke activates inflammatory cells to produce large amounts of reactive oxygen species in the lungs. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone, a potent and prevalent nitrosamine procarcinogen found in cigarette smoke, has been used extensively to study tobacco carcinogen-induced lung tumors in rodents and revealed to stimulate the survival and proliferation of lung cancer cells
  • Many studies have indicated that the 5-year survival rate of patients with lung cancer is closely related to the time of diagnosis
  • Prx3 acts as a mitochondrial scavenger of ROS, protects mitochondria against oxidative damage, and influences diverse cellular processes, including growth, differentiation, apoptosis, and carcinogenesis
  • Our results showed that NNK induces expression alterations in Prx genes over the course of lung cancer, which means Prxs may play important roles in ROS detoxification under NNK stress and be compensatory functionally
  • The genes displayed different expression patterns and showed similar responses to different concentrations of NNK. These results suggest that Prxs may play important roles in ROS detoxification under NNK stress and be compensatory functionally
  • Our results are consistent with this previous study and showed upregulation of Prx3 and Prx5 expression relative to the control after treatment with 0.3 and 0.2 mg/mL NNK

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