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    <identifier>10.57760/sciencedb.03716</identifier>
    <datestamp>2022-10-18T21:32:01Z</datestamp>
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  <dc:date>2022-10-18</dc:date>
  <dc:title>Targeting Nrf2-mediated heme oxygenase-1 enhances non-thermal plasmainduced cell death in non-small-cell lung cancer A549 cells</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.03716</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Non-thermal plasma (NTP) treatment has been proposed as a potential approach for cancer therapy for killing cancer cells via generation of reactive oxygen species (ROS). As an antioxidant protein, Heme oxygenase-1 (HO-1) has been known to protect cells against oxidative stress. In this paper, we investigated the role of HO-1 activation in NTP-induced apoptosis in A549 cells. Distinctly increased ROS production and apoptosis were observed after NTP exposure. NTP exposure induced HO-1 expression in a dose- and time-dependent manner via activating the translocation of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) from cytoplasm to nucleus. Furthermore, inhibiting HO-1 activation with its specific inhibitor, ZnPP, increased &amp;quot;killing&amp;quot; effect of NTP. Knocking down HO-1 or Nrf2 with the special siRNA also led to elevated ROS level and enhanced NTP-induced cell death. In addition, the c-JUN N-terminal kinase (JNK) signaling pathway was shown to be involved in NTP-induced HO-1 expression. Interestingly, a higher resistance to NTP exposure of A549 cell compared to H1299 and H322 cells was found to be linked to its higher basal level of HO-1 expression. These findings revealed that HO-1 could be considered as a potential target to improve the effect of NTP in cancer therapy.</dc:description>
  <dc:subject>Non-thermal plasma; Heme oxygenase-1; Apoptotic death; Reactive oxygen species; c-JUN N-terminal kinase</dc:subject>
  <dc:creator>ma jie</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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