Inhibition of eIF2α dephosphorylation accelerates pterostilbene-induced cell death in human hepatocellular carcinoma cells in an ER stress and autophagy-dependent manner
Identifieur interne : 000726 ( Main/Exploration ); précédent : 000725; suivant : 000727Inhibition of eIF2α dephosphorylation accelerates pterostilbene-induced cell death in human hepatocellular carcinoma cells in an ER stress and autophagy-dependent manner
Auteurs : Chen-Lin Yu [Taïwan] ; Shun-Fa Yang [Taïwan] ; Tung-Wei Hung [Taïwan] ; Chia-Liang Lin [Taïwan] ; Yi-Hsien Hsieh [Taïwan] ; Hui-Ling Chiou [Taïwan]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2019.
Abstract
Hepatocellular carcinoma (HCC) is the one of the most common cancers worldwide. Because the side effects of current treatments are severe, new effective therapeutic strategies are urgently required. Pterostilbene (PT), a natural analogue of resveratrol, has diverse pharmacologic activities, including antioxidative, anti-inflammatory and antiproliferative activities. Here we demonstrated that PT inhibits HCC cell growth without the induction of apoptosis in an endoplasmic reticulum (ER) stress- and autophagy-dependent manner. Mechanistic studies indicated that the combination of salubrinal and PT modulates ER stress-related autophagy through the phospho-eukaryotic initiation factor 2α/activating transcription factor-4/LC3 pathway, leading to a further inhibition of eIF2α dephosphorylation and the potentiation of cell death. An in vivo xenograft analysis revealed that PT significantly reduced tumour growth in mice with a SK-Hep-1 tumour xenograft. Taken together, our results yield novel insights into the pivotal roles of PT in ER stress- and autophagy-dependent cell death in HCC cells.
Url:
DOI: 10.1038/s41419-019-1639-5
PubMed: 31138785
PubMed Central: 6538697
Affiliations:
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Ling" sort="Chiou, Hui Ling" uniqKey="Chiou H" first="Hui-Ling" last="Chiou">Hui-Ling Chiou</name><affiliation wicri:level="1"><nlm:aff id="Aff7"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0532 2041</institution-id><institution-id institution-id-type="GRID">grid.411641.7</institution-id><institution>School of Medical Laboratory and Biotechnology,</institution><institution>Chung Shan Medical University,</institution></institution-wrap>Taichung, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Taichung</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff8"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0638 9256</institution-id><institution-id institution-id-type="GRID">grid.411645.3</institution-id><institution>Department of Clinical Laboratory,</institution><institution>Chung Shan Medical University Hospital,</institution></institution-wrap>Taichung, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Taichung</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Hepatocellular carcinoma (HCC) is the one of the most common cancers worldwide. Because the side effects of current treatments are severe, new effective therapeutic strategies are urgently required. Pterostilbene (PT), a natural analogue of resveratrol, has diverse pharmacologic activities, including antioxidative, anti-inflammatory and antiproliferative activities. Here we demonstrated that PT inhibits HCC cell growth without the induction of apoptosis in an endoplasmic reticulum (ER) stress- and autophagy-dependent manner. Mechanistic studies indicated that the combination of salubrinal and PT modulates ER stress-related autophagy through the phospho-eukaryotic initiation factor 2α/activating transcription factor-4/LC3 pathway, leading to a further inhibition of eIF2α dephosphorylation and the potentiation of cell death. An in vivo xenograft analysis revealed that PT significantly reduced tumour growth in mice with a SK-Hep-1 tumour xenograft. Taken together, our results yield novel insights into the pivotal roles of PT in ER stress- and autophagy-dependent cell death in HCC cells.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="El Serag, Hb" uniqKey="El Serag H">HB El-Serag</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Buendia, Ma" uniqKey="Buendia M">MA Buendia</name></author><author><name sortKey="Neuveut, C" uniqKey="Neuveut C">C Neuveut</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rimando, Am" uniqKey="Rimando A">AM Rimando</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Estrela, Jm" uniqKey="Estrela J">JM Estrela</name></author><author><name sortKey="Ortega, A" uniqKey="Ortega A">A Ortega</name></author><author><name sortKey="Mena, S" uniqKey="Mena S">S Mena</name></author><author><name sortKey="Rodriguez, Ml" uniqKey="Rodriguez M">ML 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uniqKey="Cullinan S">SB Cullinan</name></author><author><name sortKey="Diehl, Ja" uniqKey="Diehl J">JA Diehl</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chevet, E" uniqKey="Chevet E">E Chevet</name></author><author><name sortKey="Hetz, C" uniqKey="Hetz C">C Hetz</name></author><author><name sortKey="Samali, A" uniqKey="Samali A">A Samali</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Noh, Mr" uniqKey="Noh M">MR Noh</name></author><author><name sortKey="Woo, Ch" uniqKey="Woo C">CH Woo</name></author><author><name sortKey="Park, Mj" uniqKey="Park M">MJ Park</name></author><author><name sortKey="In Kim, J" uniqKey="In Kim J">J In Kim</name></author><author><name sortKey="Park, Km" uniqKey="Park K">KM Park</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kang, X" uniqKey="Kang X">X Kang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tsai, Tc" uniqKey="Tsai T">TC Tsai</name></author><author><name sortKey="Lai, Kh" uniqKey="Lai K">KH Lai</name></author><author><name sortKey="Su, Jh" uniqKey="Su J">JH Su</name></author><author><name sortKey="Wu, Yj" uniqKey="Wu Y">YJ Wu</name></author><author><name sortKey="Sheu, Jh" uniqKey="Sheu J">JH Sheu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Boyce, M" uniqKey="Boyce M">M Boyce</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Teng, Y" uniqKey="Teng Y">Y Teng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jeon, Yj" uniqKey="Jeon Y">YJ Jeon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, L" uniqKey="Wu L">L Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kapetanovic, Im" uniqKey="Kapetanovic I">IM Kapetanovic</name></author><author><name sortKey="Muzzio, M" uniqKey="Muzzio M">M Muzzio</name></author><author><name sortKey="Huang, Z" uniqKey="Huang Z">Z Huang</name></author><author><name sortKey="Thompson, Tn" uniqKey="Thompson T">TN Thompson</name></author><author><name sortKey="Mccormick, Dl" uniqKey="Mccormick D">DL McCormick</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wakimoto, R" uniqKey="Wakimoto R">R Wakimoto</name></author><author><name sortKey="Ono, M" uniqKey="Ono M">M Ono</name></author><author><name sortKey="Takeshima, M" uniqKey="Takeshima M">M Takeshima</name></author><author><name sortKey="Higuchi, T" uniqKey="Higuchi T">T Higuchi</name></author><author><name sortKey="Nakano, S" uniqKey="Nakano S">S Nakano</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Riche, Dm" uniqKey="Riche D">DM Riche</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Yu, Chen Lin" sort="Yu, Chen Lin" uniqKey="Yu C" first="Chen-Lin" last="Yu">Chen-Lin Yu</name></noRegion><name sortKey="Chiou, Hui Ling" sort="Chiou, Hui Ling" uniqKey="Chiou H" first="Hui-Ling" last="Chiou">Hui-Ling Chiou</name><name sortKey="Chiou, Hui Ling" sort="Chiou, Hui Ling" uniqKey="Chiou H" first="Hui-Ling" last="Chiou">Hui-Ling Chiou</name><name sortKey="Hsieh, Yi Hsien" sort="Hsieh, Yi Hsien" uniqKey="Hsieh Y" first="Yi-Hsien" last="Hsieh">Yi-Hsien Hsieh</name><name sortKey="Hsieh, Yi Hsien" sort="Hsieh, Yi Hsien" uniqKey="Hsieh Y" first="Yi-Hsien" last="Hsieh">Yi-Hsien Hsieh</name><name sortKey="Hsieh, Yi Hsien" sort="Hsieh, Yi Hsien" uniqKey="Hsieh Y" first="Yi-Hsien" last="Hsieh">Yi-Hsien Hsieh</name><name sortKey="Hung, Tung Wei" sort="Hung, Tung Wei" uniqKey="Hung T" first="Tung-Wei" last="Hung">Tung-Wei Hung</name><name sortKey="Hung, Tung Wei" sort="Hung, Tung Wei" uniqKey="Hung T" first="Tung-Wei" last="Hung">Tung-Wei Hung</name><name sortKey="Lin, Chia Liang" sort="Lin, Chia Liang" uniqKey="Lin C" first="Chia-Liang" last="Lin">Chia-Liang Lin</name><name sortKey="Yang, Shun Fa" sort="Yang, Shun Fa" uniqKey="Yang S" first="Shun-Fa" last="Yang">Shun-Fa Yang</name><name sortKey="Yang, Shun Fa" sort="Yang, Shun Fa" uniqKey="Yang S" first="Shun-Fa" last="Yang">Shun-Fa Yang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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