Tubeimoside-I sensitizes colorectal cancer cells to chemotherapy by inducing ROS-mediated impaired autophagolysosomes accumulation
Identifieur interne : 000305 ( Main/Exploration ); précédent : 000304; suivant : 000306Tubeimoside-I sensitizes colorectal cancer cells to chemotherapy by inducing ROS-mediated impaired autophagolysosomes accumulation
Auteurs : Jianghong Yan [République populaire de Chine] ; Xiaoyun Dou [République populaire de Chine] ; Jing Zhou [République populaire de Chine] ; Yuanfeng Xiong [République populaire de Chine] ; Ling Mo [République populaire de Chine] ; Longhao Li [République populaire de Chine] ; Yunlong Lei [République populaire de Chine]Source :
- Journal of Experimental & Clinical Cancer Research : CR [ 0392-9078 ] ; 2019.
Abstract
Tubeimoside-I (TBM), a plant-derived bioactive compound, shows antitumor activity in different tumors and can enhance the efficacy of chemotherapeutic agents. However, the detail mechanism underlying remains to be elucidated.
The cytotoxic potential of TBM towards CRC cells was examined by CCK8 assay, colony formation, LDH release assay, flow cytometry method and Western blots. The ROS levels, autophagy, apoptosis, chemosensitivity to 5-FU or DOX, etc. were determined between control and TBM-treated CRC cells.
In this study, we found that TBM could inhibit proliferation and induce apoptosis in colorectal cancer (CRC) cells. Intriguingly, TBM treatment could either promote autophagy initiation by ROS-induced AMPK activation, or block autophagy flux through inhibiting lysosomal hydrolytic enzymes, which leaded to massive impaired autophagylysosomes accumulation. Administration of autophagy initiation inhibitor (3-MA or selective ablation of autophagy related proteins) relieves TBM-induced CRC suppression, while combination use of autophagy flux inhibitor chloroquine (CQ) slightly augments TBM-induced cell death, suggesting that impaired autophagylysosomes accumulation contributes to TBM-induced growth inhibition in CRC cells. Notably, as an autophagy flux inhibitor, TBM works synergistically with 5-fluorouracil (5-FU) or doxorubicin (DOX) in CRC suppression.
Together, our study provides new insights regarding the anti-tumor activity of TBM against CRC, and established potential applications of TBM for CRC combination therapies in clinic.
The online version of this article (10.1186/s13046-019-1355-0) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s13046-019-1355-0
PubMed: 31412953
PubMed Central: 6694658
Affiliations:
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Center,</institution><institution>Chongqing Medical University,</institution></institution-wrap>Chongqing, 400016 People’s Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chongqing</wicri:regionArea></affiliation></author><author><name sortKey="Xiong, Yuanfeng" sort="Xiong, Yuanfeng" uniqKey="Xiong Y" first="Yuanfeng" last="Xiong">Yuanfeng Xiong</name><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0000 8653 0555</institution-id><institution-id institution-id-type="GRID">grid.203458.8</institution-id><institution>Department of Medical Laboratory Technology,</institution><institution>Chongqing Medical University,</institution></institution-wrap>Chongqing, 400016 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chongqing</wicri:regionArea></affiliation></author><author><name sortKey="Mo, Ling" sort="Mo, Ling" 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400016 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chongqing</wicri:regionArea></affiliation></author><author><name sortKey="Lei, Yunlong" sort="Lei, Yunlong" uniqKey="Lei Y" first="Yunlong" last="Lei">Yunlong Lei</name><affiliation wicri:level="1"><nlm:aff id="Aff4"><institution-wrap><institution-id institution-id-type="ISNI">0000 0000 8653 0555</institution-id><institution-id institution-id-type="GRID">grid.203458.8</institution-id><institution>Department of Biochemistry and Molecular Biology and Molecular Medicine and Cancer Research Center,</institution><institution>Chongqing Medical University,</institution></institution-wrap>Chongqing, 400016 People’s Republic of China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Chongqing</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">Tubeimoside-I (TBM), a plant-derived bioactive compound, shows antitumor activity in different tumors and can enhance the efficacy of chemotherapeutic agents. However, the detail mechanism underlying remains to be elucidated.</p></sec><sec><title>Methods</title><p id="Par2">The cytotoxic potential of TBM towards CRC cells was examined by CCK8 assay, colony formation, LDH release assay, flow cytometry method and Western blots. The ROS levels, autophagy, apoptosis, chemosensitivity to 5-FU or DOX, etc. were determined between control and TBM-treated CRC cells.</p></sec><sec><title>Results</title><p id="Par3">In this study, we found that TBM could inhibit proliferation and induce apoptosis in colorectal cancer (CRC) cells. Intriguingly, TBM treatment could either promote autophagy initiation by ROS-induced AMPK activation, or block autophagy flux through inhibiting lysosomal hydrolytic enzymes, which leaded to massive impaired autophagylysosomes accumulation. Administration of autophagy initiation inhibitor (3-MA or selective ablation of autophagy related proteins) relieves TBM-induced CRC suppression, while combination use of autophagy flux inhibitor chloroquine (CQ) slightly augments TBM-induced cell death, suggesting that impaired autophagylysosomes accumulation contributes to TBM-induced growth inhibition in CRC cells. Notably, as an autophagy flux inhibitor, TBM works synergistically with 5-fluorouracil (5-FU) or doxorubicin (DOX) in CRC suppression.</p></sec><sec><title>Conclusion</title><p id="Par4">Together, our study provides new insights regarding the anti-tumor activity of TBM against CRC, and established potential applications of TBM for CRC combination therapies in clinic.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s13046-019-1355-0) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Siegel, Rl" uniqKey="Siegel R">RL Siegel</name></author><author><name sortKey="Miller, Kd" uniqKey="Miller K">KD Miller</name></author><author><name sortKey="Fedewa, Sa" uniqKey="Fedewa S">SA Fedewa</name></author><author><name sortKey="Ahnen, Dj" uniqKey="Ahnen D">DJ Ahnen</name></author><author><name 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He</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, J" uniqKey="Kim J">J Kim</name></author><author><name sortKey="Kundu, M" uniqKey="Kundu M">M Kundu</name></author><author><name sortKey="Viollet, B" uniqKey="Viollet B">B Viollet</name></author><author><name sortKey="Guan, Kl" uniqKey="Guan K">KL Guan</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="Yan, Jianghong" sort="Yan, Jianghong" uniqKey="Yan J" first="Jianghong" last="Yan">Jianghong Yan</name></noRegion><name sortKey="Dou, Xiaoyun" sort="Dou, Xiaoyun" uniqKey="Dou X" first="Xiaoyun" last="Dou">Xiaoyun Dou</name><name sortKey="Lei, Yunlong" sort="Lei, Yunlong" uniqKey="Lei Y" first="Yunlong" last="Lei">Yunlong Lei</name><name sortKey="Li, Longhao" sort="Li, Longhao" uniqKey="Li L" first="Longhao" last="Li">Longhao Li</name><name sortKey="Mo, Ling" sort="Mo, Ling" uniqKey="Mo L" first="Ling" last="Mo">Ling Mo</name><name sortKey="Xiong, Yuanfeng" sort="Xiong, Yuanfeng" uniqKey="Xiong Y" first="Yuanfeng" last="Xiong">Yuanfeng Xiong</name><name sortKey="Yan, Jianghong" sort="Yan, Jianghong" uniqKey="Yan J" first="Jianghong" last="Yan">Jianghong Yan</name><name sortKey="Zhou, Jing" sort="Zhou, Jing" uniqKey="Zhou J" first="Jing" last="Zhou">Jing Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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