ATF4 contributes to autophagy and survival in sunitinib treated brain tumor initiating cells (BTICs).
作者： Sylvia Moeckel , Kelly LaFrance , Julia Wetsch , Corinna Seliger , Markus J. Riemenschneider
DOI: 10.18632/ONCOTARGET.26569
关键词: Autophagy 、 Sunitinib 、 Cell growth 、 Lysosome 、 Cancer research 、 Downregulation and upregulation 、 Progenitor cell 、 Small interfering RNA 、 Receptor tyrosine kinase 、 Biology
摘要: Receptor tyrosine kinase (RTK) pathways are known to play an important role in tumor cell proliferation of glioblastoma (GBM). Cellular determinants RTK-inhibitor sensitivity optimize and tailor treatment strategies. The stress response gene activating transcription factor 4 (ATF4) is involved homeostasis cellular protection. However, little about its function GBM. We found that the ATF4/p-eIF2α pathway activated Sunitinib primary initiating progenitor cultures (BTICs). Furthermore, lysosome entrapment RTK-inhibitors (RTK-Is) leads accumulation autophagosomes. In case treated cells, autophagy additionally increased by ATF4 mediated upregulation genes. Inhibition small interfering RNA (siRNA) reduced after a subset BTIC cultures. Overall, this study suggests pro-survival type specific manner.
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