Inhibition of autophagy and enhancement of endoplasmic reticulum stress increase sensitivity of osteosarcoma Saos‐2 cells to cannabinoid receptor agonist WIN55,212‐2
Identifieur interne : 000E08 ( Main/Exploration ); précédent : 000E07; suivant : 000E09Inhibition of autophagy and enhancement of endoplasmic reticulum stress increase sensitivity of osteosarcoma Saos‐2 cells to cannabinoid receptor agonist WIN55,212‐2
Auteurs : Guodong Zhang [République populaire de Chine] ; Haiyong Bi [République populaire de Chine] ; Ji Gao [République populaire de Chine] ; Xing Lu [République populaire de Chine] ; Yanping Zheng [République populaire de Chine]Source :
- Cell Biochemistry and Function [ 0263-6484 ] ; 2016-07.
Abstract
WIN55,212‐2, a cannabinoid receptor agonist, can activate cannabinoid receptors, which has proven anti‐tumour effects in several tumour types. Studies showed that WIN can inhibit tumour cell proliferation and induce apoptosis in diverse cancers. However, the role and mechanism of WIN in osteosarcoma are still unclear. In this study, we examined the effect of WIN55,212‐2 on osteosarcoma cell line Saos‐2 in terms of cell viability and apoptosis. Meanwhile, we further explored the role of endoplasmic reticulum stress and autophagy in apoptosis induced by WIN55,212‐2. Our results showed that the cell proliferation of Saos‐2 was inhibited by WIN55,212‐2 in a dose‐dependent and time‐dependent manner. WIN55,212‐2‐induced Saos‐2 apoptosis through mitochondrial apoptosis pathway. Meanwhile, WIN55,212‐2 can induce endoplasmic reticulum stress and autophagy in Saos‐2 cells. Inhibition of autophagy and enhancement of endoplasmic reticulum stress increased apoptosis induced by WIN55,212‐2 in Saos‐2 cells. These findings indicated that WIN55,212‐2 in combination with autophagic inhibitor or endoplasmic reticulum stress activator may shed new light on osteosarcoma treatment. Copyright © 2016 John Wiley & Sons, Ltd.
Url:
DOI: 10.1002/cbf.3194
Affiliations:
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receptor agonist, can activate cannabinoid receptors, which has proven anti‐tumour effects in several tumour types. Studies showed that WIN can inhibit tumour cell proliferation and induce apoptosis in diverse cancers. However, the role and mechanism of WIN in osteosarcoma are still unclear. In this study, we examined the effect of WIN55,212‐2 on osteosarcoma cell line Saos‐2 in terms of cell viability and apoptosis. Meanwhile, we further explored the role of endoplasmic reticulum stress and autophagy in apoptosis induced by WIN55,212‐2. Our results showed that the cell proliferation of Saos‐2 was inhibited by WIN55,212‐2 in a dose‐dependent and time‐dependent manner. WIN55,212‐2‐induced Saos‐2 apoptosis through mitochondrial apoptosis pathway. Meanwhile, WIN55,212‐2 can induce endoplasmic reticulum stress and autophagy in Saos‐2 cells. Inhibition of autophagy and enhancement of endoplasmic reticulum stress increased apoptosis induced by WIN55,212‐2 in Saos‐2 cells. These findings indicated that WIN55,212‐2 in combination with autophagic inhibitor or endoplasmic reticulum stress activator may shed new light on osteosarcoma treatment. Copyright © 2016 John Wiley & Sons, Ltd.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Guodong" sort="Zhang, Guodong" uniqKey="Zhang G" first="Guodong" last="Zhang">Guodong Zhang</name></noRegion><name sortKey="Bi, Haiyong" sort="Bi, Haiyong" uniqKey="Bi H" first="Haiyong" last="Bi">Haiyong Bi</name><name sortKey="Gao, Ji" sort="Gao, Ji" uniqKey="Gao J" first="Ji" last="Gao">Ji Gao</name><name sortKey="Lu, Xing" sort="Lu, Xing" uniqKey="Lu X" first="Xing" last="Lu">Xing Lu</name><name sortKey="Zhang, Guodong" sort="Zhang, Guodong" uniqKey="Zhang G" first="Guodong" last="Zhang">Guodong Zhang</name><name sortKey="Zheng, Yanping" sort="Zheng, Yanping" uniqKey="Zheng Y" first="Yanping" last="Zheng">Yanping Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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