Blocking Hypoxia-Induced Autophagy in Tumors Restores Cytotoxic T-Cell Activity and Promotes Regression
Identifieur interne : 001600 ( Main/Exploration ); précédent : 001599; suivant : 001601Blocking Hypoxia-Induced Autophagy in Tumors Restores Cytotoxic T-Cell Activity and Promotes Regression
Auteurs : MUHAMMAD ZAEEM NOMAN [France] ; Bassam Janji [Luxembourg (pays)] ; Bozena Kaminska [Pologne] ; Kris Van Moer [Luxembourg (pays)] ; Sandrine Pierson [Luxembourg (pays)] ; Piotr Przanowski [Pologne] ; Stéphanie Buart [France] ; Guy Berchem [Luxembourg (pays)] ; Pedro Romero [Suisse] ; Fathia Mami-Chouaib [France] ; Salem Chouaib [France]Source :
- Cancer research : (Baltimore) [ 0008-5472 ] ; 2011.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Oxygène.
English descriptors
- KwdEn :
Abstract
The relationship between hypoxic stress, autophagy, and specific cell-mediated cytotoxicity remains unknown. This study shows that hypoxia-induced resistance of lung tumor to cytolytic T lymphocyte (CTL)-mediated lysis is associated with autophagy induction in target cells. In turn, this correlates with STAT3 phosphorylation on tyrosine 705 residue (pSTAT3) and HIF-1α accumulation. Inhibition of autophagy by siRNA targeting of either beclin1 or Atg5 resulted in impairment of pSTAT3 and restoration of hypoxic tumor cell susceptibility to CTL-mediated lysis. Furthermore, inhibition of pSTAT3 in hypoxic Atg5 or beclin1-targeted tumor cells was found to be associated with the inhibition Src kinase (pSrc). Autophagy-induced pSTAT3 and pSrc regulation seemed to involve the ubiquitin proteasome system and p62/SQSTM1. In vivo experiments using B16-F10 melanoma tumor cells indicated that depletion of beclin1 resulted in an inhibition of B16-F10 tumor growth and increased tumor apoptosis. Moreover, in vivo inhibition of autophagy by hydroxychloroquine in B16-F10 tumor-bearing mice and mice vaccinated with tyrosinase-related protein-2 peptide dramatically increased tumor growth inhibition. Collectively, this study establishes a novel functional link between hypoxia-induced autophagy and the regulation of antigen-specific T-cell lysis and points to a major role of autophagy in the control of in vivo tumor growth.
Affiliations:
Links toward previous steps (curation, corpus...)
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy</term>
<term>Biological activity</term>
<term>Cytotoxic T lymphocyte</term>
<term>Hypoxia</term>
<term>Malignant tumor</term>
<term>Oxygen</term>
<term>Regression</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Hypoxie</term>
<term>Autophagie</term>
<term>Tumeur maligne</term>
<term>Lymphocyte T cytotoxique</term>
<term>Activité biologique</term>
<term>Régression</term>
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<front><div type="abstract" xml:lang="en">The relationship between hypoxic stress, autophagy, and specific cell-mediated cytotoxicity remains unknown. This study shows that hypoxia-induced resistance of lung tumor to cytolytic T lymphocyte (CTL)-mediated lysis is associated with autophagy induction in target cells. In turn, this correlates with STAT3 phosphorylation on tyrosine 705 residue (pSTAT3) and HIF-1α accumulation. Inhibition of autophagy by siRNA targeting of either beclin1 or Atg5 resulted in impairment of pSTAT3 and restoration of hypoxic tumor cell susceptibility to CTL-mediated lysis. Furthermore, inhibition of pSTAT3 in hypoxic Atg5 or beclin1-targeted tumor cells was found to be associated with the inhibition Src kinase (pSrc). Autophagy-induced pSTAT3 and pSrc regulation seemed to involve the ubiquitin proteasome system and p62/SQSTM1. In vivo experiments using B16-F10 melanoma tumor cells indicated that depletion of beclin1 resulted in an inhibition of B16-F10 tumor growth and increased tumor apoptosis. Moreover, in vivo inhibition of autophagy by hydroxychloroquine in B16-F10 tumor-bearing mice and mice vaccinated with tyrosinase-related protein-2 peptide dramatically increased tumor growth inhibition. Collectively, this study establishes a novel functional link between hypoxia-induced autophagy and the regulation of antigen-specific T-cell lysis and points to a major role of autophagy in the control of in vivo tumor growth.</div>
</front>
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