Different role o f Raptor and Rictor in regulating rasfonin-induced autophagy and apoptosis in renal carcinoma cells.
Identifieur interne : 000128 ( Main/Exploration ); précédent : 000127; suivant : 000129Different role o f Raptor and Rictor in regulating rasfonin-induced autophagy and apoptosis in renal carcinoma cells.
Auteurs : Xuejun Jiang [République populaire de Chine] ; Bolin Hou [République populaire de Chine] ; Shuchun Liu [République populaire de Chine] ; Erwei Li [République populaire de Chine]Source :
- Chemistry & biodiversity [ 1612-1880 ] ; 2020.
Abstract
Both Raptor and Rictor are the key components in the complexes of mammalian target of rapamycin (mTOR) , which play a vital role in mediating autophagy. Unlike mTOR, the regulatory role of either Raptor or Rictor in the regulation of autophagic process is relatively less explored. In present study, we found that rasfonin, which isolated from Talaromyces sp. 3656-A1 and was a fungal natural product, activated both caspase-dependent apoptosis and autophagy in ACHN, a renal carcinoma cell line. Knockdown of Raptor decreased both rasfonin-induced autophagic flux and PARP-1 cleavage, and in contrast, Rictor silencing increased apoptosis concomitantly enhancing rasfonin-induced autophagy. Unexpectedly, API-2, which was widely used an inhibitor of Akt, promoted rasfonin-dependent autophagy in Raptor-depleted but not Rictor-deprived cells. Collectively, these results demonstrated that Raptor and Rictor could play a distinctly regulatory role in rasfonin-enhanced autophagy and apoptosis .
DOI: 10.1002/cbdv.202000743
PubMed: 33155352
Affiliations:
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last="Liu">Shuchun Liu</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing, CHINA.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Li, Erwei" sort="Li, Erwei" uniqKey="Li E" first="Erwei" last="Li">Erwei Li</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing, CHINA.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Chemistry & biodiversity</title><idno type="eISSN">1612-1880</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Both Raptor and Rictor are the key components in the complexes of mammalian target of rapamycin (mTOR) , which play a vital role in mediating autophagy. Unlike mTOR, the regulatory role of either Raptor or Rictor in the regulation of autophagic process is relatively less explored. In present study, we found that rasfonin, which isolated from Talaromyces sp. 3656-A1 and was a fungal natural product, activated both caspase-dependent apoptosis and autophagy in ACHN, a renal carcinoma cell line. Knockdown of Raptor decreased both rasfonin-induced autophagic flux and PARP-1 cleavage, and in contrast, Rictor silencing increased apoptosis concomitantly enhancing rasfonin-induced autophagy. Unexpectedly, API-2, which was widely used an inhibitor of Akt, promoted rasfonin-dependent autophagy in Raptor-depleted but not Rictor-deprived cells. Collectively, these results demonstrated that Raptor and Rictor could play a distinctly regulatory role in rasfonin-enhanced autophagy and apoptosis .</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">33155352</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1612-1880</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Nov</Month><Day>05</Day></PubDate></JournalIssue><Title>Chemistry & biodiversity</Title><ISOAbbreviation>Chem Biodivers</ISOAbbreviation></Journal><ArticleTitle>Different role o f Raptor and Rictor in regulating rasfonin-induced autophagy and apoptosis in renal carcinoma cells.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1002/cbdv.202000743</ELocationID><Abstract><AbstractText>Both Raptor and Rictor are the key components in the complexes of mammalian target of rapamycin (mTOR) , which play a vital role in mediating autophagy. Unlike mTOR, the regulatory role of either Raptor or Rictor in the regulation of autophagic process is relatively less explored. In present study, we found that rasfonin, which isolated from Talaromyces sp. 3656-A1 and was a fungal natural product, activated both caspase-dependent apoptosis and autophagy in ACHN, a renal carcinoma cell line. Knockdown of Raptor decreased both rasfonin-induced autophagic flux and PARP-1 cleavage, and in contrast, Rictor silencing increased apoptosis concomitantly enhancing rasfonin-induced autophagy. Unexpectedly, API-2, which was widely used an inhibitor of Akt, promoted rasfonin-dependent autophagy in Raptor-depleted but not Rictor-deprived cells. Collectively, these results demonstrated that Raptor and Rictor could play a distinctly regulatory role in rasfonin-enhanced autophagy and apoptosis .</AbstractText><CopyrightInformation>© 2020 Wiley-VCH GmbH.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Xuejun</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Institute of Microbiology Chinese Academy of Sciences, state key laboratory of mycology, beichenxi road NO.3, 100101, Beijing, CHINA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hou</LastName><ForeName>Bolin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing, CHINA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Shuchun</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing, CHINA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Erwei</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute of Microbiology Chinese Academy of Sciences, State Key Laboratory of Mycology, 1 West Beichen Road, 100101, Beijing, CHINA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>11</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Chem Biodivers</MedlineTA><NlmUniqueID>101197449</NlmUniqueID><ISSNLinking>1612-1872</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Apoptosis</Keyword><Keyword MajorTopicYN="N">Raptor</Keyword><Keyword MajorTopicYN="N">Rictor</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">rasfonin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>09</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>11</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>11</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>11</Month><Day>6</Day><Hour>6</Hour><Minute>3</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33155352</ArticleId><ArticleId IdType="doi">10.1002/cbdv.202000743</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Jiang, Xuejun" sort="Jiang, Xuejun" uniqKey="Jiang X" first="Xuejun" last="Jiang">Xuejun Jiang</name></noRegion><name sortKey="Hou, Bolin" sort="Hou, Bolin" uniqKey="Hou B" first="Bolin" last="Hou">Bolin Hou</name><name sortKey="Li, Erwei" sort="Li, Erwei" uniqKey="Li E" first="Erwei" last="Li">Erwei Li</name><name sortKey="Liu, Shuchun" sort="Liu, Shuchun" uniqKey="Liu S" first="Shuchun" last="Liu">Shuchun Liu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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