CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers.
Identifieur interne : 000060 ( PubMed/Checkpoint ); précédent : 000059; suivant : 000061CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers.
Auteurs : Jihyun Lee [Corée du Sud] ; Ji Hoon Jung [Corée du Sud] ; Jisung Hwang [Corée du Sud] ; Ji Eon Park [Corée du Sud] ; Ju-Ha Kim [Corée du Sud] ; Woon Yi Park [Corée du Sud] ; Jin Young Suh [Corée du Sud] ; Sung-Hoon Kim [Corée du Sud]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
Though Atorvastatin has been used as a hypolipidemic agent, its anticancer mechanisms for repurposing are not fully understood so far. Thus, in the current study, its apoptotic and autophagic mechanisms were investigated in non-small cell lung cancers (NSCLCs). Atorvastatin increased cytotoxicity, sub G1 population, the number of apoptotic bodies, cleaved poly (ADP-ribose) polymerase (PARP) and caspase 3 and activated p53 in H1299, H596, and H460 cells. Notably, Atorvastatin inhibited the expression of c-Myc and induced ribosomal protein L5 and L11, but depletion of L5 reduced PARP cleavages induced by Atorvastatin rather than L11 in H1299 cells. Also, Atorvastatin increased autophagy microtubule-associated protein 1A/1B-light chain 3II (LC3 II) conversion, p62/sequestosome 1 (SQSTM1) accumulation with increased number of LC3II puncta in H1299 cells. However, late stage autophagy inhibitor chloroquine (CQ) increased cytotoxicity in Atorvastatin treated H1299 cells compared to early stage autophagy inhibitor 3-methyladenine (3-MA). Furthermore, autophagic flux assay using RFP-GFP-LC3 constructs and Lysotracker Red or acridine orange-staining demonstrated that autophagosome-lysosome fusion is blocked by Atorvastatin treatment in H1299 cells. Conversely, overexpression of CCR4-NOT transcription complex subunit 2(CNOT2) weakly reversed the ability of Atorvastatin to increase cytotoxicity, sub G1 population, cleavages of PARP and caspase 3, LC3II conversion and p62/SQSTM1 accumulation in H1299 cells. In contrast, CNOT2 depletion enhanced cleavages of PARP and caspase 3, LC3 conversion and p62/SQSTM1 accumulation in Atorvastatin treated H1299 cells. Overall, these findings suggest that CNOT2 signaling is critically involved in Atorvastatin induced apoptotic and autophagic cell death in NSCLCs.
DOI: 10.3390/cancers11101470
PubMed: 31574980
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Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Jung, Ji Hoon" sort="Jung, Ji Hoon" uniqKey="Jung J" first="Ji Hoon" last="Jung">Ji Hoon Jung</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. johnsperfume@gmail.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Hwang, Jisung" sort="Hwang, Jisung" uniqKey="Hwang J" first="Jisung" last="Hwang">Jisung Hwang</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. hjsung0103@naver.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Park, Ji Eon" sort="Park, Ji Eon" uniqKey="Park J" first="Ji Eon" last="Park">Ji Eon Park</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wdnk77@naver.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Kim, Ju Ha" sort="Kim, Ju Ha" uniqKey="Kim J" first="Ju-Ha" last="Kim">Ju-Ha Kim</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. 964juha@daum.net.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Park, Woon Yi" sort="Park, Woon Yi" uniqKey="Park W" first="Woon Yi" last="Park">Woon Yi Park</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wy1319@naver.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Suh, Jin Young" sort="Suh, Jin Young" uniqKey="Suh J" first="Jin Young" last="Suh">Jin Young Suh</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. jysuh3670@gmail.com.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author><author><name sortKey="Kim, Sung Hoon" sort="Kim, Sung Hoon" uniqKey="Kim S" first="Sung-Hoon" last="Kim">Sung-Hoon Kim</name><affiliation wicri:level="1"><nlm:affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. sungkim7@khu.ac.kr.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Korean Medicine, Kyung Hee University, Seoul 02447</wicri:regionArea><placeName><settlement type="city">Séoul</settlement><region type="capital">Région capitale de Séoul</region></placeName></affiliation></author></analytic><series><title level="j">Cancers</title><idno type="ISSN">2072-6694</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">Though Atorvastatin has been used as a hypolipidemic agent, its anticancer mechanisms for repurposing are not fully understood so far. Thus, in the current study, its apoptotic and autophagic mechanisms were investigated in non-small cell lung cancers (NSCLCs). Atorvastatin increased cytotoxicity, sub G1 population, the number of apoptotic bodies, cleaved poly (ADP-ribose) polymerase (PARP) and caspase 3 and activated p53 in H1299, H596, and H460 cells. Notably, Atorvastatin inhibited the expression of c-Myc and induced ribosomal protein L5 and L11, but depletion of L5 reduced PARP cleavages induced by Atorvastatin rather than L11 in H1299 cells. Also, Atorvastatin increased autophagy microtubule-associated protein 1A/1B-light chain 3II (LC3 II) conversion, p62/sequestosome 1 (SQSTM1) accumulation with increased number of LC3II puncta in H1299 cells. However, late stage autophagy inhibitor chloroquine (CQ) increased cytotoxicity in Atorvastatin treated H1299 cells compared to early stage autophagy inhibitor 3-methyladenine (3-MA). Furthermore, autophagic flux assay using RFP-GFP-LC3 constructs and Lysotracker Red or acridine orange-staining demonstrated that autophagosome-lysosome fusion is blocked by Atorvastatin treatment in H1299 cells. Conversely, overexpression of CCR4-NOT transcription complex subunit 2(CNOT2) weakly reversed the ability of Atorvastatin to increase cytotoxicity, sub G1 population, cleavages of PARP and caspase 3, LC3II conversion and p62/SQSTM1 accumulation in H1299 cells. In contrast, CNOT2 depletion enhanced cleavages of PARP and caspase 3, LC3 conversion and p62/SQSTM1 accumulation in Atorvastatin treated H1299 cells. Overall, these findings suggest that CNOT2 signaling is critically involved in Atorvastatin induced apoptotic and autophagic cell death in NSCLCs.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">31574980</PMID><DateRevised><Year>2019</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Print">2072-6694</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>10</Issue><PubDate><Year>2019</Year><Month>Sep</Month><Day>30</Day></PubDate></JournalIssue><Title>Cancers</Title><ISOAbbreviation>Cancers (Basel)</ISOAbbreviation></Journal><ArticleTitle>CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E1470</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/cancers11101470</ELocationID><Abstract><AbstractText>Though Atorvastatin has been used as a hypolipidemic agent, its anticancer mechanisms for repurposing are not fully understood so far. Thus, in the current study, its apoptotic and autophagic mechanisms were investigated in non-small cell lung cancers (NSCLCs). Atorvastatin increased cytotoxicity, sub G1 population, the number of apoptotic bodies, cleaved poly (ADP-ribose) polymerase (PARP) and caspase 3 and activated p53 in H1299, H596, and H460 cells. Notably, Atorvastatin inhibited the expression of c-Myc and induced ribosomal protein L5 and L11, but depletion of L5 reduced PARP cleavages induced by Atorvastatin rather than L11 in H1299 cells. Also, Atorvastatin increased autophagy microtubule-associated protein 1A/1B-light chain 3II (LC3 II) conversion, p62/sequestosome 1 (SQSTM1) accumulation with increased number of LC3II puncta in H1299 cells. However, late stage autophagy inhibitor chloroquine (CQ) increased cytotoxicity in Atorvastatin treated H1299 cells compared to early stage autophagy inhibitor 3-methyladenine (3-MA). Furthermore, autophagic flux assay using RFP-GFP-LC3 constructs and Lysotracker Red or acridine orange-staining demonstrated that autophagosome-lysosome fusion is blocked by Atorvastatin treatment in H1299 cells. Conversely, overexpression of CCR4-NOT transcription complex subunit 2(CNOT2) weakly reversed the ability of Atorvastatin to increase cytotoxicity, sub G1 population, cleavages of PARP and caspase 3, LC3II conversion and p62/SQSTM1 accumulation in H1299 cells. In contrast, CNOT2 depletion enhanced cleavages of PARP and caspase 3, LC3 conversion and p62/SQSTM1 accumulation in Atorvastatin treated H1299 cells. Overall, these findings suggest that CNOT2 signaling is critically involved in Atorvastatin induced apoptotic and autophagic cell death in NSCLCs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Jihyun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. jhlee096@naver.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jung</LastName><ForeName>Ji Hoon</ForeName><Initials>JH</Initials><Identifier Source="ORCID">0000-0002-5644-5960</Identifier><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. johnsperfume@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hwang</LastName><ForeName>Jisung</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. hjsung0103@naver.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Ji Eon</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wdnk77@naver.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Ju-Ha</ForeName><Initials>JH</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. 964juha@daum.net.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Woon Yi</ForeName><Initials>WY</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. wy1319@naver.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suh</LastName><ForeName>Jin Young</ForeName><Initials>JY</Initials><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. jysuh3670@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sung-Hoon</ForeName><Initials>SH</Initials><Identifier Source="ORCID">0000-0003-2423-1973</Identifier><AffiliationInfo><Affiliation>College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea. sungkim7@khu.ac.kr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>2017R1A2A1A17069297</GrantID><Agency>National Research Foundation of Korea</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>09</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cancers (Basel)</MedlineTA><NlmUniqueID>101526829</NlmUniqueID><ISSNLinking>2072-6694</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">CNOT2</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">atorvastatin</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">non-small lung cancer cells</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>08</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>09</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>09</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>10</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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Séoul</li></region><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><region name="Région capitale de Séoul"><name sortKey="Lee, Jihyun" sort="Lee, Jihyun" uniqKey="Lee J" first="Jihyun" last="Lee">Jihyun Lee</name></region><name sortKey="Hwang, Jisung" sort="Hwang, Jisung" uniqKey="Hwang J" first="Jisung" last="Hwang">Jisung Hwang</name><name sortKey="Jung, Ji Hoon" sort="Jung, Ji Hoon" uniqKey="Jung J" first="Ji Hoon" last="Jung">Ji Hoon Jung</name><name sortKey="Kim, Ju Ha" sort="Kim, Ju Ha" uniqKey="Kim J" first="Ju-Ha" last="Kim">Ju-Ha Kim</name><name sortKey="Kim, Sung Hoon" sort="Kim, Sung Hoon" uniqKey="Kim S" first="Sung-Hoon" last="Kim">Sung-Hoon Kim</name><name sortKey="Park, Ji Eon" sort="Park, Ji Eon" uniqKey="Park J" first="Ji Eon" last="Park">Ji Eon Park</name><name sortKey="Park, Woon Yi" sort="Park, Woon Yi" uniqKey="Park W" first="Woon Yi" last="Park">Woon Yi Park</name><name sortKey="Suh, Jin Young" sort="Suh, Jin Young" uniqKey="Suh J" 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