Autophagy inhibition enhances PD-L1 expression in gastric cancer
Identifieur interne : 000A28 ( Main/Exploration ); précédent : 000A27; suivant : 000A29Autophagy inhibition enhances PD-L1 expression in gastric cancer
Auteurs : Xiaojuan Wang [République populaire de Chine] ; William K. K. Wu [République populaire de Chine] ; Jing Gao [République populaire de Chine] ; Zhongwu Li [République populaire de Chine] ; Bin Dong [République populaire de Chine] ; Xiaoting Lin [République populaire de Chine] ; Yilin Li [République populaire de Chine] ; Yanyan Li [République populaire de Chine] ; Jifang Gong [République populaire de Chine] ; Changsong Qi [République populaire de Chine] ; Zhi Peng [République populaire de Chine] ; Jun Yu [République populaire de Chine] ; Lin Shen [République populaire de Chine]Source :
- Journal of Experimental & Clinical Cancer Research : CR [ 0392-9078 ] ; 2019.
Abstract
Autophagy, a process for degrading intracellular substances to maintain basal metabolic turnover, is known to be perturbed in gastric cancer. Programmed cell death-1 (PD-1) with its ligand (PD-L1) are important immune checkpoint proteins and their regulation by autophagy has been reported in mouse melanoma and human ovarian cancer. Here, we explored the interplay between autophagy and the PD1/PD-L1 axis in gastric cancer.
The expression of PD-L1 in gastric cancer cells was detected by Western blot and flow cytometry analysis. The effect of autophagy inhibition on PD-L1 expression was examined in vitro and in vivo. The molecular mechanisms of the regulation of PD-L1 by autophagy were evaluated in gastric cancer cell lines. The clinical relevance of autophagy-related markers p62/SQSTM1 and LC3 with PD-L1 was evaluated in 137 patients with gastric cancer.
We found that inhibition of autophagy by pharmacological inhibitors or small interfering RNAs increased the levels of PD-L1 in cultured gastric cancer cells and in xenografts. Interferon (IFN)-γ also promoted PD-L1 gene transcription, whose action was enhanced by autophagy inhibition. Mechanistically, autophagy inhibition led to the accumulation of p62/SQSTM1 and activation of nuclear factor (NF)-κB, in which NF-κB inhibition or p62/SQSTM1 knockdown attenuated PD-L1 induction by autophagy inhibition. Immunohistochemical staining of primary tumor tissues of 137 patients with gastric cancer showed that LC3 and p62/SQSTM1 protein levels were positively correlated with PD-L1 (LC3,
We discovered that autophagy regulates PD-L1 expression in gastric cancer through the p62/SQSTM1-NF-κB pathway. Pharmacological modulation of autophagy may thus influence the therapeutic efficacy of PD-L1 blockade in gastric cancer.
The online version of this article (10.1186/s13046-019-1148-5) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13046-019-1148-5
PubMed: 30925913
PubMed Central: 6440013
Affiliations:
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institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Wu, William K K" sort="Wu, William K K" uniqKey="Wu W" first="William K. K." last="Wu">William K. K. Wu</name><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0482</institution-id><institution-id institution-id-type="GRID">grid.10784.3a</institution-id><institution>Department of Anaesthesia and Intensive Care,</institution><institution>The Chinese University of Hong Kong,</institution></institution-wrap>Hong Kong, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hong Kong</wicri:regionArea></affiliation></author><author><name sortKey="Gao, Jing" sort="Gao, Jing" uniqKey="Gao J" first="Jing" last="Gao">Jing Gao</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Li, Zhongwu" sort="Li, Zhongwu" uniqKey="Li Z" first="Zhongwu" last="Li">Zhongwu Li</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Pathology,</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Dong, Bin" sort="Dong, Bin" uniqKey="Dong B" first="Bin" last="Dong">Bin Dong</name><affiliation wicri:level="1"><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Central Laboratory,</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Lin, Xiaoting" sort="Lin, Xiaoting" uniqKey="Lin X" first="Xiaoting" last="Lin">Xiaoting Lin</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Pathology,</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Li, Yilin" sort="Li, Yilin" uniqKey="Li Y" first="Yilin" last="Li">Yilin Li</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Li, Yanyan" sort="Li, Yanyan" uniqKey="Li Y" first="Yanyan" last="Li">Yanyan Li</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Gong, Jifang" sort="Gong, Jifang" uniqKey="Gong J" first="Jifang" last="Gong">Jifang Gong</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Qi, Changsong" sort="Qi, Changsong" uniqKey="Qi C" first="Changsong" last="Qi">Changsong Qi</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Peng, Zhi" sort="Peng, Zhi" uniqKey="Peng Z" first="Zhi" last="Peng">Zhi Peng</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Yu, Jun" sort="Yu, Jun" uniqKey="Yu J" first="Jun" last="Yu">Jun Yu</name><affiliation wicri:level="1"><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0482</institution-id><institution-id institution-id-type="GRID">grid.10784.3a</institution-id><institution>Department of Medicine and Therapeutics,</institution><institution>The Chinese University of Hong Kong,</institution></institution-wrap>Hong Kong, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Hong Kong</wicri:regionArea></affiliation></author><author><name sortKey="Shen, Lin" sort="Shen, Lin" uniqKey="Shen L" first="Lin" last="Shen">Lin Shen</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0027 0586</institution-id><institution-id institution-id-type="GRID">grid.412474.0</institution-id><institution>Department of Gastrointestinal Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing),</institution><institution>Peking University Cancer Hospital and Institute,</institution></institution-wrap>Beijing, 100142 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Beijing</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of Experimental & Clinical Cancer Research : CR</title><idno type="ISSN">0392-9078</idno><idno type="eISSN">1756-9966</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p id="Par1">Autophagy, a process for degrading intracellular substances to maintain basal metabolic turnover, is known to be perturbed in gastric cancer. Programmed cell death-1 (PD-1) with its ligand (PD-L1) are important immune checkpoint proteins and their regulation by autophagy has been reported in mouse melanoma and human ovarian cancer. Here, we explored the interplay between autophagy and the PD1/PD-L1 axis in gastric cancer.</p></sec><sec><title>Methods</title><p id="Par2">The expression of PD-L1 in gastric cancer cells was detected by Western blot and flow cytometry analysis. The effect of autophagy inhibition on PD-L1 expression was examined in vitro and in vivo. The molecular mechanisms of the regulation of PD-L1 by autophagy were evaluated in gastric cancer cell lines. The clinical relevance of autophagy-related markers p62/SQSTM1 and LC3 with PD-L1 was evaluated in 137 patients with gastric cancer.</p></sec><sec><title>Results</title><p id="Par3">We found that inhibition of autophagy by pharmacological inhibitors or small interfering RNAs increased the levels of PD-L1 in cultured gastric cancer cells and in xenografts. Interferon (IFN)-γ also promoted PD-L1 gene transcription, whose action was enhanced by autophagy inhibition. Mechanistically, autophagy inhibition led to the accumulation of p62/SQSTM1 and activation of nuclear factor (NF)-κB, in which NF-κB inhibition or p62/SQSTM1 knockdown attenuated PD-L1 induction by autophagy inhibition. Immunohistochemical staining of primary tumor tissues of 137 patients with gastric cancer showed that LC3 and p62/SQSTM1 protein levels were positively correlated with PD-L1 (LC3, <italic>p</italic> < 0.001; p62/SQSTM1, <italic>p</italic> < 0.05). The expression of PD-L1 was also positively correlated with tumor lymphocyte infiltration (<italic>p</italic> < 0.001).</p></sec><sec><title>Conclusions</title><p id="Par4">We discovered that autophagy regulates PD-L1 expression in gastric cancer through the p62/SQSTM1-NF-κB pathway. Pharmacological modulation of autophagy may thus influence the therapeutic efficacy of PD-L1 blockade in gastric cancer.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s13046-019-1148-5) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Torre, La" uniqKey="Torre L">LA Torre</name></author><author><name sortKey="Bray, F" uniqKey="Bray F">F Bray</name></author><author><name sortKey="Siegel, Rl" uniqKey="Siegel R">RL Siegel</name></author><author><name sortKey="Ferlay, J" uniqKey="Ferlay J">J Ferlay</name></author><author><name sortKey="Lortet Tieulent, J" uniqKey="Lortet Tieulent J">J Lortet-Tieulent</name></author><author><name sortKey="Jemal, A" uniqKey="Jemal A">A Jemal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="White, E" uniqKey="White E">E 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uniqKey="Liang X">X Liang</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Xiaojuan" sort="Wang, Xiaojuan" uniqKey="Wang X" first="Xiaojuan" last="Wang">Xiaojuan Wang</name></noRegion><name sortKey="Dong, Bin" sort="Dong, Bin" uniqKey="Dong B" first="Bin" last="Dong">Bin Dong</name><name sortKey="Gao, Jing" sort="Gao, Jing" uniqKey="Gao J" first="Jing" last="Gao">Jing Gao</name><name sortKey="Gong, Jifang" sort="Gong, Jifang" uniqKey="Gong J" first="Jifang" last="Gong">Jifang Gong</name><name sortKey="Li, Yanyan" sort="Li, Yanyan" uniqKey="Li Y" first="Yanyan" last="Li">Yanyan Li</name><name sortKey="Li, Yilin" sort="Li, Yilin" uniqKey="Li Y" first="Yilin" last="Li">Yilin Li</name><name sortKey="Li, Zhongwu" sort="Li, Zhongwu" uniqKey="Li Z" first="Zhongwu" last="Li">Zhongwu Li</name><name sortKey="Lin, Xiaoting" sort="Lin, Xiaoting" uniqKey="Lin X" first="Xiaoting" last="Lin">Xiaoting Lin</name><name sortKey="Peng, Zhi" sort="Peng, Zhi" uniqKey="Peng Z" first="Zhi" last="Peng">Zhi Peng</name><name sortKey="Qi, Changsong" sort="Qi, Changsong" uniqKey="Qi C" first="Changsong" last="Qi">Changsong Qi</name><name sortKey="Shen, Lin" sort="Shen, Lin" uniqKey="Shen L" first="Lin" last="Shen">Lin Shen</name><name sortKey="Wu, William K K" sort="Wu, William K K" uniqKey="Wu W" first="William K. K." last="Wu">William K. K. Wu</name><name sortKey="Yu, Jun" sort="Yu, Jun" uniqKey="Yu J" first="Jun" last="Yu">Jun Yu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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