Inhibition of Protein Phosphatase 1 Stimulates Noncanonical ER Stress eIF2α Activation to Enhance Fisetin-induced Chemosensitivity in HDAC Inhibitor-resistant Hepatocellular Carcinoma Cells
Identifieur interne : 000727 ( Main/Merge ); précédent : 000726; suivant : 000728Inhibition of Protein Phosphatase 1 Stimulates Noncanonical ER Stress eIF2α Activation to Enhance Fisetin-induced Chemosensitivity in HDAC Inhibitor-resistant Hepatocellular Carcinoma Cells
Auteurs : Yi-Sheng Liu [Taïwan] ; Yu-Chun Chang [Taïwan] ; Wei-Wen Kuo [Taïwan] ; Ming-Cheng Chen [Taïwan] ; Hsi-Hsien Hsu [Taïwan] ; Chuan-Chou Tu [Taïwan] ; Yu-Lan Yeh [Taïwan] ; Vijaya Padma Viswanadha [Inde] ; Po-Hsiang Liao [Taïwan] ; Chih-Yang Huang [Taïwan]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
Hepatocellular carcinoma (HCC) is a common fatal type of malignant tumor that has highly metastatic and recurrent properties. Fisetin is a natural flavonoid found in various vegetables and fruits which exhibits anti-cancer and anti-inflammatory properties, as well as other effects. Thus, we hypothesized that fisetin can act as an adjuvant therapy in cancer or drug-resistant cancer cells, and further investigated the molecular mechanisms underlying the development of drug-resistance in HCC cells. We found that fisetin effectively inhibited the cell viability of not only parental cells but also histone deacetylase inhibitors-resistant (HDACis-R) cells and enhanced the chemosensitivity of HCC cells. Interestingly, fisetin did not induce cell apoptosis through the activation of the endoplasmic reticulum (ER) stress sensor of protein kinase R (PKR)-like endoplasmic reticulum kinase, but rather through the non-canonical pathway of the protein phosphatase 1 (PP1)-mediated suppression of eIF2α phosphorylation. Moreover, fisetin-induced cell apoptosis was reversed by treatment with PP1 activator or eIF2α siRNA in HCC cells. Based on these observations, we suggest that PP1-eIF2α pathways are significantly involved in the effect of fisetin on HCC apoptosis. Thus, fisetin may act as a novel anticancer drug and new chemotherapy adjuvant which can improve the efficacy of chemotherapeutic agents and diminish their side-effects.
Url:
DOI: 10.3390/cancers11070918
PubMed: 31261976
PubMed Central: 6678694
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Inhibition of Protein Phosphatase 1 Stimulates Noncanonical ER Stress eIF2α Activation to Enhance Fisetin-induced Chemosensitivity in HDAC Inhibitor-resistant Hepatocellular Carcinoma Cells</title>
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<author><name sortKey="Kuo, Wei Wen" sort="Kuo, Wei Wen" uniqKey="Kuo W" first="Wei-Wen" last="Kuo">Wei-Wen Kuo</name>
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<author><name sortKey="Hsu, Hsi Hsien" sort="Hsu, Hsi Hsien" uniqKey="Hsu H" first="Hsi-Hsien" last="Hsu">Hsi-Hsien Hsu</name>
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<author><name sortKey="Tu, Chuan Chou" sort="Tu, Chuan Chou" uniqKey="Tu C" first="Chuan-Chou" last="Tu">Chuan-Chou Tu</name>
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<author><name sortKey="Yeh, Yu Lan" sort="Yeh, Yu Lan" uniqKey="Yeh Y" first="Yu-Lan" last="Yeh">Yu-Lan Yeh</name>
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<author><name sortKey="Viswanadha, Vijaya Padma" sort="Viswanadha, Vijaya Padma" uniqKey="Viswanadha V" first="Vijaya Padma" last="Viswanadha">Vijaya Padma Viswanadha</name>
<affiliation wicri:level="1"><nlm:aff id="af13-cancers-11-00918">Department of Biotechnology, Bharathiar University, Coimbatore 641046, India</nlm:aff>
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<author><name sortKey="Liao, Po Hsiang" sort="Liao, Po Hsiang" uniqKey="Liao P" first="Po-Hsiang" last="Liao">Po-Hsiang Liao</name>
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<author><name sortKey="Huang, Chih Yang" sort="Huang, Chih Yang" uniqKey="Huang C" first="Chih-Yang" last="Huang">Chih-Yang Huang</name>
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<affiliation wicri:level="1"><nlm:aff id="af17-cancers-11-00918">Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan</nlm:aff>
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<affiliation wicri:level="1"><nlm:aff id="af18-cancers-11-00918">Department of Biotechnology, Asia University, Taichung 413, Taiwan</nlm:aff>
<country xml:lang="fr">Taïwan</country>
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<front><div type="abstract" xml:lang="en"><p>Hepatocellular carcinoma (HCC) is a common fatal type of malignant tumor that has highly metastatic and recurrent properties. Fisetin is a natural flavonoid found in various vegetables and fruits which exhibits anti-cancer and anti-inflammatory properties, as well as other effects. Thus, we hypothesized that fisetin can act as an adjuvant therapy in cancer or drug-resistant cancer cells, and further investigated the molecular mechanisms underlying the development of drug-resistance in HCC cells. We found that fisetin effectively inhibited the cell viability of not only parental cells but also histone deacetylase inhibitors-resistant (HDACis-R) cells and enhanced the chemosensitivity of HCC cells. Interestingly, fisetin did not induce cell apoptosis through the activation of the endoplasmic reticulum (ER) stress sensor of protein kinase R (PKR)-like endoplasmic reticulum kinase, but rather through the non-canonical pathway of the protein phosphatase 1 (PP1)-mediated suppression of eIF2α phosphorylation. Moreover, fisetin-induced cell apoptosis was reversed by treatment with PP1 activator or eIF2α siRNA in HCC cells. Based on these observations, we suggest that PP1-eIF2α pathways are significantly involved in the effect of fisetin on HCC apoptosis. Thus, fisetin may act as a novel anticancer drug and new chemotherapy adjuvant which can improve the efficacy of chemotherapeutic agents and diminish their side-effects. </p>
</div>
</front>
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