Regulating autophagy facilitated therapeutic efficacy of the sonic Hedgehog pathway inhibition on lung adenocarcinoma through GLI2 suppression and ROS production.
Identifieur interne : 000031 ( PubMed/Checkpoint ); précédent : 000030; suivant : 000032Regulating autophagy facilitated therapeutic efficacy of the sonic Hedgehog pathway inhibition on lung adenocarcinoma through GLI2 suppression and ROS production.
Auteurs : Jiajun Fan [République populaire de Chine] ; Xuyao Zhang [République populaire de Chine] ; Shaofei Wang [République populaire de Chine] ; Wei Chen [République populaire de Chine] ; Yubin Li [République populaire de Chine] ; Xian Zeng [République populaire de Chine] ; Yichen Wang [République populaire de Chine] ; Jingyun Luan [République populaire de Chine] ; Li Li [République populaire de Chine] ; Ziyu Wang [République populaire de Chine] ; Xilin Sun [République populaire de Chine] ; Baozhong Shen [République populaire de Chine] ; Dianwen Ju [République populaire de Chine]Source :
- Cell death & disease [ 2041-4889 ] ; 2019.
Abstract
Lung adenocarcinoma (LUAD), which comprises over 50% of all cases of non-small-cell lung cancer, has a poor prognosis and requires novel therapeutic approaches. The sonic Hedgehog (Shh) pathway, which plays a crucial role in differentiation, proliferation, and survival of cancer cells, is likely to be activated in LUADs, suggesting the Shh pathway as a potential therapeutic target for LUAD treatment. In this study, we reported that vismodegib, an inhibitor of the Shh pathway, only elicited minor antitumor efficacy in A549 and NCI-H1975 LUAD cells as well as in the xenograft tumors, with overexpressed GLI2 and increased autophagic activity. The aberrant autophagy in LUAD cells was further confirmed by the three main stages of autophagic flux, including the formation of autophagosomes, the fusion of autophagosomes with lysosomes, and degradation of autophagosomes in lysosomes. Furthermore, inhibition of autophagy by siRNA against ATG5 or ATG7 rescued the sensitivity of A549 and NCI-H1975 LUAD cells to vismodegib in vitro. Meanwhile, administration of the pharmaceutical inhibitor of autophagy, chloroquine, contributed to the enhanced anti-LUAD efficacy of vismodegib in vivo, probably through overproduction of ROS, acceleration of apoptosis, and suppression of GLI2 in LUAD tissues. In summary, our research revealed that downregulating autophagy facilitated the anti-LUAD efficacy of the Shh pathway suppression, thus highlighting a potential approach for LUAD therapy via simultaneously targeting the Shh signaling and autophagy pathway.
DOI: 10.1038/s41419-019-1840-6
PubMed: 31427566
Affiliations:
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<front><div type="abstract" xml:lang="en">Lung adenocarcinoma (LUAD), which comprises over 50% of all cases of non-small-cell lung cancer, has a poor prognosis and requires novel therapeutic approaches. The sonic Hedgehog (Shh) pathway, which plays a crucial role in differentiation, proliferation, and survival of cancer cells, is likely to be activated in LUADs, suggesting the Shh pathway as a potential therapeutic target for LUAD treatment. In this study, we reported that vismodegib, an inhibitor of the Shh pathway, only elicited minor antitumor efficacy in A549 and NCI-H1975 LUAD cells as well as in the xenograft tumors, with overexpressed GLI2 and increased autophagic activity. The aberrant autophagy in LUAD cells was further confirmed by the three main stages of autophagic flux, including the formation of autophagosomes, the fusion of autophagosomes with lysosomes, and degradation of autophagosomes in lysosomes. Furthermore, inhibition of autophagy by siRNA against ATG5 or ATG7 rescued the sensitivity of A549 and NCI-H1975 LUAD cells to vismodegib in vitro. Meanwhile, administration of the pharmaceutical inhibitor of autophagy, chloroquine, contributed to the enhanced anti-LUAD efficacy of vismodegib in vivo, probably through overproduction of ROS, acceleration of apoptosis, and suppression of GLI2 in LUAD tissues. In summary, our research revealed that downregulating autophagy facilitated the anti-LUAD efficacy of the Shh pathway suppression, thus highlighting a potential approach for LUAD therapy via simultaneously targeting the Shh signaling and autophagy pathway.</div>
</front>
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<Abstract><AbstractText>Lung adenocarcinoma (LUAD), which comprises over 50% of all cases of non-small-cell lung cancer, has a poor prognosis and requires novel therapeutic approaches. The sonic Hedgehog (Shh) pathway, which plays a crucial role in differentiation, proliferation, and survival of cancer cells, is likely to be activated in LUADs, suggesting the Shh pathway as a potential therapeutic target for LUAD treatment. In this study, we reported that vismodegib, an inhibitor of the Shh pathway, only elicited minor antitumor efficacy in A549 and NCI-H1975 LUAD cells as well as in the xenograft tumors, with overexpressed GLI2 and increased autophagic activity. The aberrant autophagy in LUAD cells was further confirmed by the three main stages of autophagic flux, including the formation of autophagosomes, the fusion of autophagosomes with lysosomes, and degradation of autophagosomes in lysosomes. Furthermore, inhibition of autophagy by siRNA against ATG5 or ATG7 rescued the sensitivity of A549 and NCI-H1975 LUAD cells to vismodegib in vitro. Meanwhile, administration of the pharmaceutical inhibitor of autophagy, chloroquine, contributed to the enhanced anti-LUAD efficacy of vismodegib in vivo, probably through overproduction of ROS, acceleration of apoptosis, and suppression of GLI2 in LUAD tissues. In summary, our research revealed that downregulating autophagy facilitated the anti-LUAD efficacy of the Shh pathway suppression, thus highlighting a potential approach for LUAD therapy via simultaneously targeting the Shh signaling and autophagy pathway.</AbstractText>
</Abstract>
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<AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy and The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai, 201203, China.</Affiliation>
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<ForeName>Ziyu</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy and The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai, 201203, China.</Affiliation>
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<ForeName>Xilin</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>The Fourth Hospital of Harbin Medical University, Harbin, 150028, P. R. China. sunxl@ems.hrbmu.edu.cn.</Affiliation>
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<ForeName>Baozhong</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>The Fourth Hospital of Harbin Medical University, Harbin, 150028, P. R. China. shenbz@ems.hrbmu.edu.cn.</Affiliation>
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<ForeName>Dianwen</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Minhang Hospital, Fudan University, 170 Xinsong Road, Shanghai, 201199, China. dianwenju@fudan.edu.cn.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Microbiological and Biochemical Pharmacy and The Key Laboratory of Smart Drug Delivery, Ministry of Education, School of Pharmacy, Fudan University, Shanghai, 201203, China. dianwenju@fudan.edu.cn.</Affiliation>
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<Day>26</Day>
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<affiliations><list><country><li>République populaire de Chine</li>
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<name sortKey="Wang, Yichen" sort="Wang, Yichen" uniqKey="Wang Y" first="Yichen" last="Wang">Yichen Wang</name>
<name sortKey="Wang, Ziyu" sort="Wang, Ziyu" uniqKey="Wang Z" first="Ziyu" last="Wang">Ziyu Wang</name>
<name sortKey="Zeng, Xian" sort="Zeng, Xian" uniqKey="Zeng X" first="Xian" last="Zeng">Xian Zeng</name>
<name sortKey="Zhang, Xuyao" sort="Zhang, Xuyao" uniqKey="Zhang X" first="Xuyao" last="Zhang">Xuyao Zhang</name>
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