Blocking Hypoxia-Induced Autophagy in Tumors Restores Cytotoxic T-Cell Activity and Promotes Regression
Identifieur interne : 000053 ( PascalFrancis/Curation ); précédent : 000052; suivant : 000054Blocking 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.
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</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Autophagie</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Autophagy</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Autofagia</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Tumeur maligne</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Malignant tumor</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Tumor maligno</s0>
<s2>NM</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Lymphocyte T cytotoxique</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Cytotoxic T lymphocyte</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Linfocito T citotóxico</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Activité biologique</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Biological activity</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Actividad biológica</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Régression</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Regression</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Regresión</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Oxygène</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>23</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Oxygen</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>23</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Oxígeno</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>23</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cancer</s0>
<s2>NM</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Cáncer</s0>
<s2>NM</s2>
</fC07>
<fN21><s1>297</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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