CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers
Identifieur interne : 000982 ( Main/Exploration ); précédent : 000981; suivant : 000983CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers
Auteurs : Jihyun Lee ; Ji Hoon Jung ; Jisung Hwang ; Ji Eon Park ; Ju-Ha Kim ; Woon Yi Park ; Jin Young Suh ; Sung-Hoon KimSource :
- 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.
Url:
DOI: 10.3390/cancers11101470
PubMed: 31574980
PubMed Central: 6826547
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers</title><author><name sortKey="Lee, Jihyun" sort="Lee, Jihyun" uniqKey="Lee J" first="Jihyun" last="Lee">Jihyun Lee</name></author><author><name sortKey="Jung, Ji Hoon" sort="Jung, Ji Hoon" uniqKey="Jung J" first="Ji Hoon" last="Jung">Ji Hoon Jung</name></author><author><name sortKey="Hwang, Jisung" sort="Hwang, Jisung" uniqKey="Hwang J" first="Jisung" last="Hwang">Jisung Hwang</name></author><author><name sortKey="Park, Ji Eon" sort="Park, Ji Eon" uniqKey="Park J" first="Ji Eon" last="Park">Ji Eon Park</name></author><author><name sortKey="Kim, Ju Ha" sort="Kim, Ju Ha" uniqKey="Kim J" first="Ju-Ha" last="Kim">Ju-Ha Kim</name></author><author><name sortKey="Park, Woon Yi" sort="Park, Woon Yi" uniqKey="Park W" first="Woon Yi" last="Park">Woon Yi Park</name></author><author><name sortKey="Suh, Jin Young" sort="Suh, Jin Young" uniqKey="Suh J" first="Jin Young" last="Suh">Jin Young Suh</name></author><author><name sortKey="Kim, Sung Hoon" sort="Kim, Sung Hoon" uniqKey="Kim S" first="Sung-Hoon" last="Kim">Sung-Hoon Kim</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31574980</idno><idno type="pmc">6826547</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6826547</idno><idno type="RBID">PMC:6826547</idno><idno type="doi">10.3390/cancers11101470</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000458</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000458</idno><idno type="wicri:Area/Pmc/Curation">000458</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000458</idno><idno type="wicri:Area/Pmc/Checkpoint">000918</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000918</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">000030</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000030</idno><idno type="wicri:Area/PubMed/Curation">000030</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000030</idno><idno type="wicri:Area/PubMed/Checkpoint">000060</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000060</idno><idno type="wicri:Area/Ncbi/Merge">000A72</idno><idno type="wicri:Area/Ncbi/Curation">000A72</idno><idno type="wicri:Area/Ncbi/Checkpoint">000A72</idno><idno type="wicri:Area/Main/Merge">000982</idno><idno type="wicri:Area/Main/Curation">000982</idno><idno type="wicri:Area/Main/Exploration">000982</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">CNOT2 Is Critically Involved in Atorvastatin Induced Apoptotic and Autophagic Cell Death in Non-Small Cell Lung Cancers</title><author><name sortKey="Lee, Jihyun" sort="Lee, Jihyun" uniqKey="Lee J" first="Jihyun" last="Lee">Jihyun Lee</name></author><author><name sortKey="Jung, Ji Hoon" sort="Jung, Ji Hoon" uniqKey="Jung J" first="Ji Hoon" last="Jung">Ji Hoon Jung</name></author><author><name sortKey="Hwang, Jisung" sort="Hwang, Jisung" uniqKey="Hwang J" first="Jisung" last="Hwang">Jisung Hwang</name></author><author><name sortKey="Park, Ji Eon" sort="Park, Ji Eon" uniqKey="Park J" first="Ji Eon" last="Park">Ji Eon Park</name></author><author><name sortKey="Kim, Ju Ha" sort="Kim, Ju Ha" uniqKey="Kim J" first="Ju-Ha" last="Kim">Ju-Ha Kim</name></author><author><name sortKey="Park, Woon Yi" sort="Park, Woon Yi" uniqKey="Park W" first="Woon Yi" last="Park">Woon Yi Park</name></author><author><name sortKey="Suh, Jin Young" sort="Suh, Jin Young" uniqKey="Suh J" first="Jin Young" last="Suh">Jin Young Suh</name></author><author><name sortKey="Kim, Sung Hoon" sort="Kim, Sung Hoon" uniqKey="Kim S" first="Sung-Hoon" last="Kim">Sung-Hoon Kim</name></author></analytic><series><title level="j">Cancers</title><idno type="eISSN">2072-6694</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Hirsch, F R" uniqKey="Hirsch F">F.R. 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Kim</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><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="Lee, Jihyun" sort="Lee, Jihyun" uniqKey="Lee J" first="Jihyun" last="Lee">Jihyun Lee</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" first="Jin Young" last="Suh">Jin Young Suh</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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