Revisiting autophagy addiction of tumor cells

Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported t...

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Bibliographic Details
Published inAutophagy Vol. 12; no. 7; pp. 1206 - 1207
Main Authors Nyfeler, Beat, Eng, Christina H.
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 02.07.2016
Subjects
Animals
Antirheumatic Agents - pharmacology
ATG7
Autophagic Puncta
autophagy
Autophagy - drug effects
cancer
Cell Line, Tumor
chloroquine
Chloroquine - pharmacology
Humans
KRAS
Proto-Oncogene Proteins p21(ras) - metabolism
chloroquine
KRAS
cancer
autophagy
ATG7
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Summary:Inhibition of autophagy has been widely explored as a potential therapeutic intervention for cancer. Different factors such as tumor origin, tumor stage and genetic background can define a tumor's response to autophagy modulation. Notably, tumors with oncogenic mutations in KRAS were reported to depend on macroautophagy in order to cope with oncogene-induced metabolic stress. Our recent report details the unexpected finding that autophagy is dispensable for KRAS-driven tumor growth in vitro and in vivo. Additionally, we clarify that the antitumorigenic effects of chloroquine, a frequently used nonspecific inhibitor of autophagy, are not connected to the inhibition of macroautophagy. Our data suggest that caution should be exercised when using chloroquine and its analogs to decipher the roles of autophagy in cancer.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
ISSN:1554-8627
1554-8635
DOI:10.1080/15548627.2016.1170265