Inhibition of autophagy potentiates the anti-metastasis effect of phenethyl isothiocyanate through JAK2/STAT3 pathway in lung cancer cells.
Identifieur interne : 000C30 ( Main/Exploration ); précédent : 000C29; suivant : 000C31Inhibition of autophagy potentiates the anti-metastasis effect of phenethyl isothiocyanate through JAK2/STAT3 pathway in lung cancer cells.
Auteurs : Huimin Wang [République populaire de Chine] ; Limin Wang [République populaire de Chine] ; Limin Cao [République populaire de Chine] ; Qicheng Zhang [République populaire de Chine] ; Qianqian Song [République populaire de Chine] ; Zhaowei Meng [République populaire de Chine] ; Xiang Wu [République populaire de Chine] ; Ke Xu [République populaire de Chine]Source :
- Molecular carcinogenesis [ 1098-2744 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Anticarcinogènes (), Anticarcinogènes (administration et posologie), Anticarcinogènes (pharmacologie), Autophagie (), Autophagie (génétique), Bécline-1 (génétique), Bécline-1 (métabolisme), Cellules A549, Facteur de transcription STAT-3 (métabolisme), Humains, Interférence par ARN, Isothiocyanates (), Isothiocyanates (administration et posologie), Isothiocyanates (pharmacologie), Kinase Janus-2 (métabolisme), Lignée cellulaire tumorale, Mouvement cellulaire (), Mouvement cellulaire (génétique), Métastase tumorale, Souris, Structure moléculaire, Tests d'activité antitumorale sur modèle de xénogreffe (), Transduction du signal (), Tumeurs du poumon (génétique), Tumeurs du poumon (métabolisme), Tumeurs du poumon (traitement médicamenteux).
- MESH :
- administration et posologie : Anticarcinogènes, Isothiocyanates.
- génétique : Autophagie, Bécline-1, Mouvement cellulaire, Tumeurs du poumon.
- métabolisme : Bécline-1, Facteur de transcription STAT-3, Kinase Janus-2, Tumeurs du poumon.
- pharmacologie : Anticarcinogènes, Isothiocyanates.
- traitement médicamenteux : Tumeurs du poumon.
- Animaux, Anticarcinogènes, Autophagie, Cellules A549, Humains, Interférence par ARN, Isothiocyanates, Lignée cellulaire tumorale, Mouvement cellulaire, Métastase tumorale, Souris, Structure moléculaire, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.
English descriptors
- KwdEn :
- A549 Cells, Animals, Anticarcinogenic Agents (administration & dosage), Anticarcinogenic Agents (chemistry), Anticarcinogenic Agents (pharmacology), Autophagy (drug effects), Autophagy (genetics), Beclin-1 (genetics), Beclin-1 (metabolism), Cell Line, Tumor, Cell Movement (drug effects), Cell Movement (genetics), Humans, Isothiocyanates (administration & dosage), Isothiocyanates (chemistry), Isothiocyanates (pharmacology), Janus Kinase 2 (metabolism), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Mice, Molecular Structure, Neoplasm Metastasis, RNA Interference, STAT3 Transcription Factor (metabolism), Signal Transduction (drug effects), Xenograft Model Antitumor Assays (methods).
- MESH :
- chemical , administration & dosage : Anticarcinogenic Agents, Isothiocyanates.
- chemical , chemistry : Anticarcinogenic Agents, Isothiocyanates.
- chemical , genetics : Beclin-1.
- chemical , metabolism : Beclin-1, Janus Kinase 2, STAT3 Transcription Factor.
- chemical , pharmacology : Anticarcinogenic Agents, Isothiocyanates.
- drug effects : Autophagy, Cell Movement, Signal Transduction.
- drug therapy : Lung Neoplasms.
- genetics : Autophagy, Cell Movement, Lung Neoplasms.
- metabolism : Lung Neoplasms.
- methods : Xenograft Model Antitumor Assays.
- A549 Cells, Animals, Cell Line, Tumor, Humans, Mice, Molecular Structure, Neoplasm Metastasis, RNA Interference.
Abstract
Phenethyl isothiocyanate (PEITC) is a natural compound abundant in cruciferous vegetables. PEITC possesses anti-tumor effect in various human malignances. Our previous study has shown that benzyl isothiocyanates (BITC) induce autophagy in lung cancer cells. However, whether autophagy play a role in the inhibitory effect of PEITC on lung cancer metastasis is unclear. In this study, we found that PEITC suppressed migration and invasion of lung cancer cells by regulating MMP2. It also induced autophagy, evidenced by the formation of acidic vesicular organelles (AVOs), the punctate pattern of LC3, the accumulation of LC3-II, and the expression of Beclin-1. Inhibition of autophagy by 3-MA and chloroquine (CQ) or knock down of Beclin-1 enhanced PEITC-caused metastasis inhibition. JAK2/STAT3 pathway was suppressed by PEITC, and further inhibited by 3-MA and CQ or Beclin-1 knock down, as a result of decreased expression of p-JAK2 and p-STAT3. Blocking JAK2/STAT3 pathway by inhibitor AG490 and Stattic suppressed cell migration and decreased the expression of MMP2, MMP9, Twist, and c-Myc. Further in vivo study showed that PEITC inhibited tumor growth, induced autophagy and suppressed JAK2/STAT3 pathway, and inhibitor CQ enhanced this effect. Taken together, our results demonstrate that PEITC inhibits metastasis potential of lung cancer cells, and induces autophagy. The autophagy induced by PEITC preserves metastasis potential of lung cancer cells, via activation of JAK2/STAT3 pathway. Inhibition of autophagy enhanced the inhibitory effect of PEITC on metastasis potential of lung cancer cells. Our finding suggests that targeting autophagy could be a promising strategy for anti-metastasis therapies.
DOI: 10.1002/mc.22777
PubMed: 29278657
Affiliations:
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Le document en format XML
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University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author><author><name sortKey="Wang, Limin" sort="Wang, Limin" uniqKey="Wang L" first="Limin" last="Wang">Limin Wang</name><affiliation wicri:level="3"><nlm:affiliation>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author><author><name sortKey="Cao, Limin" sort="Cao, Limin" uniqKey="Cao L" first="Limin" last="Cao">Limin Cao</name><affiliation wicri:level="3"><nlm:affiliation>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author><author><name sortKey="Zhang, Qicheng" sort="Zhang, Qicheng" uniqKey="Zhang Q" first="Qicheng" last="Zhang">Qicheng Zhang</name><affiliation wicri:level="3"><nlm:affiliation>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author><author><name sortKey="Song, Qianqian" sort="Song, Qianqian" uniqKey="Song Q" first="Qianqian" last="Song">Qianqian Song</name><affiliation wicri:level="3"><nlm:affiliation>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer 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Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Core Facility Center, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author><author><name sortKey="Xu, Ke" sort="Xu, Ke" uniqKey="Xu K" first="Ke" last="Xu">Ke Xu</name><affiliation wicri:level="3"><nlm:affiliation>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenviroment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin</wicri:regionArea><placeName><settlement type="city">Tianjin</settlement></placeName></affiliation></author></analytic><series><title level="j">Molecular carcinogenesis</title><idno type="eISSN">1098-2744</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Anticarcinogenic Agents (administration & dosage)</term><term>Anticarcinogenic Agents (chemistry)</term><term>Anticarcinogenic Agents (pharmacology)</term><term>Autophagy (drug effects)</term><term>Autophagy (genetics)</term><term>Beclin-1 (genetics)</term><term>Beclin-1 (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Movement (drug effects)</term><term>Cell Movement (genetics)</term><term>Humans</term><term>Isothiocyanates (administration & dosage)</term><term>Isothiocyanates (chemistry)</term><term>Isothiocyanates (pharmacology)</term><term>Janus Kinase 2 (metabolism)</term><term>Lung Neoplasms (drug therapy)</term><term>Lung Neoplasms (genetics)</term><term>Lung Neoplasms (metabolism)</term><term>Mice</term><term>Molecular Structure</term><term>Neoplasm Metastasis</term><term>RNA Interference</term><term>STAT3 Transcription Factor (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Xenograft Model Antitumor Assays (methods)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticarcinogènes ()</term><term>Anticarcinogènes (administration et posologie)</term><term>Anticarcinogènes (pharmacologie)</term><term>Autophagie ()</term><term>Autophagie (génétique)</term><term>Bécline-1 (génétique)</term><term>Bécline-1 (métabolisme)</term><term>Cellules A549</term><term>Facteur de transcription STAT-3 (métabolisme)</term><term>Humains</term><term>Interférence par ARN</term><term>Isothiocyanates ()</term><term>Isothiocyanates (administration et posologie)</term><term>Isothiocyanates (pharmacologie)</term><term>Kinase Janus-2 (métabolisme)</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire ()</term><term>Mouvement cellulaire (génétique)</term><term>Métastase tumorale</term><term>Souris</term><term>Structure moléculaire</term><term>Tests d'activité antitumorale sur modèle de xénogreffe ()</term><term>Transduction du signal ()</term><term>Tumeurs du poumon (génétique)</term><term>Tumeurs du poumon (métabolisme)</term><term>Tumeurs du poumon (traitement médicamenteux)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Anticarcinogenic Agents</term><term>Isothiocyanates</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Anticarcinogenic Agents</term><term>Isothiocyanates</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Beclin-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>Janus Kinase 2</term><term>STAT3 Transcription Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anticarcinogenic Agents</term><term>Isothiocyanates</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Anticarcinogènes</term><term>Isothiocyanates</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Movement</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term><term>Cell Movement</term><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term><term>Bécline-1</term><term>Mouvement cellulaire</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung Neoplasms</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Xenograft Model Antitumor Assays</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term><term>Facteur de transcription STAT-3</term><term>Kinase Janus-2</term><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anticarcinogènes</term><term>Isothiocyanates</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Cell Line, Tumor</term><term>Humans</term><term>Mice</term><term>Molecular Structure</term><term>Neoplasm Metastasis</term><term>RNA Interference</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Anticarcinogènes</term><term>Autophagie</term><term>Cellules A549</term><term>Humains</term><term>Interférence par ARN</term><term>Isothiocyanates</term><term>Lignée cellulaire tumorale</term><term>Mouvement cellulaire</term><term>Métastase tumorale</term><term>Souris</term><term>Structure moléculaire</term><term>Tests d'activité antitumorale sur modèle de xénogreffe</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Phenethyl isothiocyanate (PEITC) is a natural compound abundant in cruciferous vegetables. PEITC possesses anti-tumor effect in various human malignances. Our previous study has shown that benzyl isothiocyanates (BITC) induce autophagy in lung cancer cells. However, whether autophagy play a role in the inhibitory effect of PEITC on lung cancer metastasis is unclear. In this study, we found that PEITC suppressed migration and invasion of lung cancer cells by regulating MMP2. It also induced autophagy, evidenced by the formation of acidic vesicular organelles (AVOs), the punctate pattern of LC3, the accumulation of LC3-II, and the expression of Beclin-1. Inhibition of autophagy by 3-MA and chloroquine (CQ) or knock down of Beclin-1 enhanced PEITC-caused metastasis inhibition. JAK2/STAT3 pathway was suppressed by PEITC, and further inhibited by 3-MA and CQ or Beclin-1 knock down, as a result of decreased expression of p-JAK2 and p-STAT3. Blocking JAK2/STAT3 pathway by inhibitor AG490 and Stattic suppressed cell migration and decreased the expression of MMP2, MMP9, Twist, and c-Myc. Further in vivo study showed that PEITC inhibited tumor growth, induced autophagy and suppressed JAK2/STAT3 pathway, and inhibitor CQ enhanced this effect. Taken together, our results demonstrate that PEITC inhibits metastasis potential of lung cancer cells, and induces autophagy. The autophagy induced by PEITC preserves metastasis potential of lung cancer cells, via activation of JAK2/STAT3 pathway. Inhibition of autophagy enhanced the inhibitory effect of PEITC on metastasis potential of lung cancer cells. Our finding suggests that targeting autophagy could be a promising strategy for anti-metastasis therapies.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Tianjin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Huimin" sort="Wang, Huimin" uniqKey="Wang H" first="Huimin" last="Wang">Huimin Wang</name></noRegion><name sortKey="Cao, Limin" sort="Cao, Limin" uniqKey="Cao L" first="Limin" last="Cao">Limin Cao</name><name sortKey="Meng, Zhaowei" sort="Meng, Zhaowei" uniqKey="Meng Z" first="Zhaowei" last="Meng">Zhaowei Meng</name><name sortKey="Song, Qianqian" sort="Song, Qianqian" uniqKey="Song Q" first="Qianqian" last="Song">Qianqian Song</name><name sortKey="Wang, Limin" sort="Wang, Limin" uniqKey="Wang L" first="Limin" last="Wang">Limin Wang</name><name sortKey="Wu, Xiang" sort="Wu, Xiang" uniqKey="Wu X" first="Xiang" last="Wu">Xiang Wu</name><name sortKey="Xu, Ke" sort="Xu, Ke" uniqKey="Xu K" first="Ke" last="Xu">Ke Xu</name><name sortKey="Zhang, Qicheng" sort="Zhang, Qicheng" uniqKey="Zhang Q" first="Qicheng" last="Zhang">Qicheng Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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