Sufentanil impairs autophagic degradation and inhibits cell migration in NCI-H460 in vitro.
Identifieur interne : 000027 ( PubMed/Checkpoint ); précédent : 000026; suivant : 000028Sufentanil impairs autophagic degradation and inhibits cell migration in NCI-H460 in vitro.
Auteurs : Hui Jiang [République populaire de Chine] ; Hongxian Wang [République populaire de Chine] ; Weiwei Zou [République populaire de Chine] ; Yuexia Hu [République populaire de Chine] ; Chen Chen [République populaire de Chine] ; Chunhui Wang [République populaire de Chine]Source :
- Oncology letters [ 1792-1074 ] ; 2019.
Abstract
Metastasis, which involves the spread of cancer cells to distant tissues and organs, is a major cause of cancer-associated mortality. Although the use of anesthetics and analgesics may affect cancer cell metastasis, the underlying molecular mechanism remains unclear. Autophagy is a lysosome-based dynamic intracellular catabolic process that serves a crucial role in cancer cell metastasis. In order to investigate the role of autophagy in the migration of cancer cells treated with analgesics, immunofluorescence, western blotting, wound healing assay and cell invasion assay were performed in the present study. The results from immunofluorescence and western blotting demonstrated that the opioid analgesic sufentanil stimulated LC3 induction in NCI-H460 cells. Furthermore, sufentanil increased LC3 and Beclin1 protein levels, but inhibited the fusion of autophagosomes and lysosomes. In addition, sufentanil decreased cathepsin D protein level and increased p62 protein level. The addition of chloroquine (CQ) to sufentanil did not induce a further increase in LC3-II protein levels in NCI-H460 cells, suggesting the impairment of autophagic degradation. Furthermore, treatment with trehalose stimulated the migration of sufentanil-treated cells, whereas additional treatment with CQ did not further decrease the migration of sufentanil-treated cells. In addition, sufentanil co-treatment with trehalose significantly increased the invasion of lung cancer cells, whereas, additional treatment with CQ did not further reduce the invasion of sufentanil-treated cells. These results indicated that autophagy may be involved in the inhibition of NCI-H460 cell migration by sufentanil, and that sufentanil may be considered as a favorable analgesic for patients with lung cancer.
DOI: 10.3892/ol.2019.10997
PubMed: 31788126
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author><author><name sortKey="Wang, Hongxian" sort="Wang, Hongxian" uniqKey="Wang H" first="Hongxian" last="Wang">Hongxian Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author><author><name sortKey="Zou, Weiwei" sort="Zou, Weiwei" uniqKey="Zou W" first="Weiwei" last="Zou">Weiwei Zou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author><author><name sortKey="Hu, Yuexia" sort="Hu, Yuexia" uniqKey="Hu Y" first="Yuexia" last="Hu">Yuexia Hu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author><author><name sortKey="Chen, Chen" sort="Chen, Chen" uniqKey="Chen C" first="Chen" last="Chen">Chen Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author><author><name sortKey="Wang, Chunhui" sort="Wang, Chunhui" uniqKey="Wang C" first="Chunhui" last="Wang">Chunhui Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032</wicri:regionArea><placeName><settlement type="city">Hefei</settlement><region type="province">Anhui</region></placeName></affiliation></author></analytic><series><title level="j">Oncology letters</title><idno type="ISSN">1792-1074</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Metastasis, which involves the spread of cancer cells to distant tissues and organs, is a major cause of cancer-associated mortality. Although the use of anesthetics and analgesics may affect cancer cell metastasis, the underlying molecular mechanism remains unclear. Autophagy is a lysosome-based dynamic intracellular catabolic process that serves a crucial role in cancer cell metastasis. In order to investigate the role of autophagy in the migration of cancer cells treated with analgesics, immunofluorescence, western blotting, wound healing assay and cell invasion assay were performed in the present study. The results from immunofluorescence and western blotting demonstrated that the opioid analgesic sufentanil stimulated LC3 induction in NCI-H460 cells. Furthermore, sufentanil increased LC3 and Beclin1 protein levels, but inhibited the fusion of autophagosomes and lysosomes. In addition, sufentanil decreased cathepsin D protein level and increased p62 protein level. The addition of chloroquine (CQ) to sufentanil did not induce a further increase in LC3-II protein levels in NCI-H460 cells, suggesting the impairment of autophagic degradation. Furthermore, treatment with trehalose stimulated the migration of sufentanil-treated cells, whereas additional treatment with CQ did not further decrease the migration of sufentanil-treated cells. In addition, sufentanil co-treatment with trehalose significantly increased the invasion of lung cancer cells, whereas, additional treatment with CQ did not further reduce the invasion of sufentanil-treated cells. These results indicated that autophagy may be involved in the inhibition of NCI-H460 cell migration by sufentanil, and that sufentanil may be considered as a favorable analgesic for patients with lung cancer.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">31788126</PMID><DateRevised><Year>2020</Year><Month>03</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1792-1074</ISSN><JournalIssue CitedMedium="Print"><Volume>18</Volume><Issue>6</Issue><PubDate><Year>2019</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Oncology letters</Title><ISOAbbreviation>Oncol Lett</ISOAbbreviation></Journal><ArticleTitle>Sufentanil impairs autophagic degradation and inhibits cell migration in NCI-H460 <i>in vitro</i>.</ArticleTitle><Pagination><MedlinePgn>6829-6835</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3892/ol.2019.10997</ELocationID><Abstract><AbstractText>Metastasis, which involves the spread of cancer cells to distant tissues and organs, is a major cause of cancer-associated mortality. Although the use of anesthetics and analgesics may affect cancer cell metastasis, the underlying molecular mechanism remains unclear. Autophagy is a lysosome-based dynamic intracellular catabolic process that serves a crucial role in cancer cell metastasis. In order to investigate the role of autophagy in the migration of cancer cells treated with analgesics, immunofluorescence, western blotting, wound healing assay and cell invasion assay were performed in the present study. The results from immunofluorescence and western blotting demonstrated that the opioid analgesic sufentanil stimulated LC3 induction in NCI-H460 cells. Furthermore, sufentanil increased LC3 and Beclin1 protein levels, but inhibited the fusion of autophagosomes and lysosomes. In addition, sufentanil decreased cathepsin D protein level and increased p62 protein level. The addition of chloroquine (CQ) to sufentanil did not induce a further increase in LC3-II protein levels in NCI-H460 cells, suggesting the impairment of autophagic degradation. Furthermore, treatment with trehalose stimulated the migration of sufentanil-treated cells, whereas additional treatment with CQ did not further decrease the migration of sufentanil-treated cells. In addition, sufentanil co-treatment with trehalose significantly increased the invasion of lung cancer cells, whereas, additional treatment with CQ did not further reduce the invasion of sufentanil-treated cells. These results indicated that autophagy may be involved in the inhibition of NCI-H460 cell migration by sufentanil, and that sufentanil may be considered as a favorable analgesic for patients with lung cancer.</AbstractText><CopyrightInformation>Copyright: © Jiang et al.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Hui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Hongxian</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zou</LastName><ForeName>Weiwei</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hu</LastName><ForeName>Yuexia</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Chen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Chunhui</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, The Fourth Affiliated Hospital of Anhui Medical University, Anhui, Hefei 20032, P.R. China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>10</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>Greece</Country><MedlineTA>Oncol Lett</MedlineTA><NlmUniqueID>101531236</NlmUniqueID><ISSNLinking>1792-1074</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">cancer cell migration</Keyword><Keyword MajorTopicYN="N">sufentanil</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>10</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>08</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>12</Month><Day>4</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31788126</ArticleId><ArticleId IdType="doi">10.3892/ol.2019.10997</ArticleId><ArticleId IdType="pii">OL-0-0-10997</ArticleId><ArticleId IdType="pmc">PMC6865617</ArticleId></ArticleIdList><pmc-dir>pmcsd</pmc-dir>
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HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:31788126" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a ChloroquineV1
| This area was generated with Dilib version V0.6.33. |  |