The checkpoint 1 kinase inhibitor LY2603618 induces cell cycle arrest, DNA damage response and autophagy in cancer cells.
Identifieur interne : 000290 ( PubMed/Corpus ); précédent : 000289; suivant : 000291The checkpoint 1 kinase inhibitor LY2603618 induces cell cycle arrest, DNA damage response and autophagy in cancer cells.
Auteurs : Feng-Ze Wang ; Hong-Rong Fei ; Ying-Jie Cui ; Ying-Kun Sun ; Zhao-Mei Li ; Xue-Ying Wang ; Xiao-Yi Yang ; Ji-Guo Zhang ; Bao-Liang SunSource :
- Apoptosis : an international journal on programmed cell death [ 1573-675X ] ; 2014.
English descriptors
- KwdEn :
- Antineoplastic Agents (pharmacology), Antirheumatic Agents (pharmacology), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung, Caspases (metabolism), Cell Line, Tumor (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Checkpoint Kinase 1, Chloroquine (pharmacology), DNA Damage, DNA Repair (drug effects), G2 Phase Cell Cycle Checkpoints, Humans, Lung Neoplasms, MAP Kinase Kinase 4 (metabolism), Nuclear Proteins (metabolism), Phenylurea Compounds (pharmacology), Phosphorylation (drug effects), Protein Kinase Inhibitors (pharmacology), Protein Kinases (metabolism), Pyrazines (pharmacology), Serine (metabolism), p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , metabolism : Caspases, MAP Kinase Kinase 4, Nuclear Proteins, Protein Kinases, Serine, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Antineoplastic Agents, Antirheumatic Agents, Chloroquine, Phenylurea Compounds, Protein Kinase Inhibitors, Pyrazines.
- drug effects : Autophagy, Cell Line, Tumor, Cell Proliferation, Cell Survival, DNA Repair, Phosphorylation.
- Carcinoma, Non-Small-Cell Lung, Checkpoint Kinase 1, DNA Damage, G2 Phase Cell Cycle Checkpoints, Humans, Lung Neoplasms.
Abstract
Chemotherapy- or radiotherapy-induced DNA damage activates the Chk1-dependent DNA damage response (DDR) and cell cycle checkpoints to facilitate cell survival. Numerous attempts have been made to identify specific Chk1 inhibitors to enhance the efficiency of chemotherapy or radiotherapy. In this study, we investigated the molecular mechanisms underlying the antitumor activity of LY2603618, a potent and selective small molecule inhibitor of Chk1 protein kinase, in human lung cancer cells. Treatment of cancer cells with LY2603618 caused cell cycle arrest in the G2/M phase. A marked induction of DDR, including the phosphorylation of ATM, Chk2, p53 and histone H2AX, was observed after LY2603618 treatment. LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1). In addition, LY2603618-treated lung cancer cells transitioned from LC3-I to LC3-II, a hallmark of autophagy. Blocking autophagy with chloroquine (CQ) further enhanced LY2603618's inhibitory effect on cell viability/proliferation. LY2603618 also significantly increased p38 and c-Jun N-terminal kinase (JNK) phosphorylation. Pretreatment with the JNK inhibitor reduced cleavage of caspase-3 and PARP levels in LY2603618-treated cells. These results suggest the following: (i) the biological consequences of LY2603618 in lung cancer cells is associated with both inhibition of Chk1 phosphorylation on S296 and activation of the DNA damage response network; and (ii) the anticancer property of LY2603618 might be increased by inhibiting autophagy.
DOI: 10.1007/s10495-014-1010-3
PubMed: 24928205
Links to Exploration step
pubmed:24928205Le document en format XML
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Li</name></author><author><name sortKey="Wang, Xue Ying" sort="Wang, Xue Ying" uniqKey="Wang X" first="Xue-Ying" last="Wang">Xue-Ying Wang</name></author><author><name sortKey="Yang, Xiao Yi" sort="Yang, Xiao Yi" uniqKey="Yang X" first="Xiao-Yi" last="Yang">Xiao-Yi Yang</name></author><author><name sortKey="Zhang, Ji Guo" sort="Zhang, Ji Guo" uniqKey="Zhang J" first="Ji-Guo" last="Zhang">Ji-Guo Zhang</name></author><author><name sortKey="Sun, Bao Liang" sort="Sun, Bao Liang" uniqKey="Sun B" first="Bao-Liang" last="Sun">Bao-Liang Sun</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24928205</idno><idno type="pmid">24928205</idno><idno type="doi">10.1007/s10495-014-1010-3</idno><idno type="wicri:Area/PubMed/Corpus">000290</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000290</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The checkpoint 1 kinase inhibitor LY2603618 induces cell cycle arrest, DNA damage response and autophagy in cancer cells.</title><author><name sortKey="Wang, Feng Ze" sort="Wang, Feng Ze" uniqKey="Wang F" first="Feng-Ze" last="Wang">Feng-Ze Wang</name><affiliation><nlm:affiliation>School of Biological Science, Taishan Medical University, Taian, 271016, People's Republic of China.</nlm:affiliation></affiliation></author><author><name sortKey="Fei, Hong Rong" sort="Fei, Hong Rong" uniqKey="Fei H" first="Hong-Rong" last="Fei">Hong-Rong Fei</name></author><author><name sortKey="Cui, Ying Jie" sort="Cui, Ying Jie" uniqKey="Cui Y" first="Ying-Jie" last="Cui">Ying-Jie Cui</name></author><author><name sortKey="Sun, Ying Kun" sort="Sun, Ying Kun" uniqKey="Sun Y" first="Ying-Kun" last="Sun">Ying-Kun Sun</name></author><author><name sortKey="Li, Zhao Mei" sort="Li, Zhao Mei" uniqKey="Li Z" first="Zhao-Mei" last="Li">Zhao-Mei Li</name></author><author><name sortKey="Wang, Xue Ying" sort="Wang, Xue Ying" uniqKey="Wang X" first="Xue-Ying" last="Wang">Xue-Ying Wang</name></author><author><name sortKey="Yang, Xiao Yi" sort="Yang, Xiao Yi" uniqKey="Yang X" first="Xiao-Yi" last="Yang">Xiao-Yi Yang</name></author><author><name sortKey="Zhang, Ji Guo" sort="Zhang, Ji Guo" uniqKey="Zhang J" first="Ji-Guo" last="Zhang">Ji-Guo Zhang</name></author><author><name sortKey="Sun, Bao Liang" sort="Sun, Bao Liang" uniqKey="Sun B" first="Bao-Liang" last="Sun">Bao-Liang Sun</name></author></analytic><series><title level="j">Apoptosis : an international journal on programmed cell death</title><idno type="eISSN">1573-675X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antineoplastic Agents (pharmacology)</term><term>Antirheumatic Agents (pharmacology)</term><term>Autophagy (drug effects)</term><term>Carcinoma, Non-Small-Cell Lung</term><term>Caspases (metabolism)</term><term>Cell Line, Tumor (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Checkpoint Kinase 1</term><term>Chloroquine (pharmacology)</term><term>DNA Damage</term><term>DNA Repair (drug effects)</term><term>G2 Phase Cell Cycle Checkpoints</term><term>Humans</term><term>Lung Neoplasms</term><term>MAP Kinase Kinase 4 (metabolism)</term><term>Nuclear Proteins (metabolism)</term><term>Phenylurea Compounds (pharmacology)</term><term>Phosphorylation (drug effects)</term><term>Protein Kinase Inhibitors (pharmacology)</term><term>Protein Kinases (metabolism)</term><term>Pyrazines (pharmacology)</term><term>Serine (metabolism)</term><term>p38 Mitogen-Activated Protein Kinases (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term><term>MAP Kinase Kinase 4</term><term>Nuclear Proteins</term><term>Protein Kinases</term><term>Serine</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term><term>Antirheumatic Agents</term><term>Chloroquine</term><term>Phenylurea Compounds</term><term>Protein Kinase Inhibitors</term><term>Pyrazines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Cell Survival</term><term>DNA Repair</term><term>Phosphorylation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term><term>Checkpoint Kinase 1</term><term>DNA Damage</term><term>G2 Phase Cell Cycle Checkpoints</term><term>Humans</term><term>Lung Neoplasms</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chemotherapy- or radiotherapy-induced DNA damage activates the Chk1-dependent DNA damage response (DDR) and cell cycle checkpoints to facilitate cell survival. Numerous attempts have been made to identify specific Chk1 inhibitors to enhance the efficiency of chemotherapy or radiotherapy. In this study, we investigated the molecular mechanisms underlying the antitumor activity of LY2603618, a potent and selective small molecule inhibitor of Chk1 protein kinase, in human lung cancer cells. Treatment of cancer cells with LY2603618 caused cell cycle arrest in the G2/M phase. A marked induction of DDR, including the phosphorylation of ATM, Chk2, p53 and histone H2AX, was observed after LY2603618 treatment. LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1). In addition, LY2603618-treated lung cancer cells transitioned from LC3-I to LC3-II, a hallmark of autophagy. Blocking autophagy with chloroquine (CQ) further enhanced LY2603618's inhibitory effect on cell viability/proliferation. LY2603618 also significantly increased p38 and c-Jun N-terminal kinase (JNK) phosphorylation. Pretreatment with the JNK inhibitor reduced cleavage of caspase-3 and PARP levels in LY2603618-treated cells. These results suggest the following: (i) the biological consequences of LY2603618 in lung cancer cells is associated with both inhibition of Chk1 phosphorylation on S296 and activation of the DNA damage response network; and (ii) the anticancer property of LY2603618 might be increased by inhibiting autophagy. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24928205</PMID><DateCompleted><Year>2015</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-675X</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>9</Issue><PubDate><Year>2014</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Apoptosis : an international journal on programmed cell death</Title><ISOAbbreviation>Apoptosis</ISOAbbreviation></Journal><ArticleTitle>The checkpoint 1 kinase inhibitor LY2603618 induces cell cycle arrest, DNA damage response and autophagy in cancer cells.</ArticleTitle><Pagination><MedlinePgn>1389-98</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s10495-014-1010-3</ELocationID><Abstract><AbstractText>Chemotherapy- or radiotherapy-induced DNA damage activates the Chk1-dependent DNA damage response (DDR) and cell cycle checkpoints to facilitate cell survival. Numerous attempts have been made to identify specific Chk1 inhibitors to enhance the efficiency of chemotherapy or radiotherapy. In this study, we investigated the molecular mechanisms underlying the antitumor activity of LY2603618, a potent and selective small molecule inhibitor of Chk1 protein kinase, in human lung cancer cells. Treatment of cancer cells with LY2603618 caused cell cycle arrest in the G2/M phase. A marked induction of DDR, including the phosphorylation of ATM, Chk2, p53 and histone H2AX, was observed after LY2603618 treatment. LY2603618 inhibited Chk1 autophosphorylation (S296 Chk1) and increased DNA damage-mediated Chk1 phosphorylation (S345 Chk1). In addition, LY2603618-treated lung cancer cells transitioned from LC3-I to LC3-II, a hallmark of autophagy. Blocking autophagy with chloroquine (CQ) further enhanced LY2603618's inhibitory effect on cell viability/proliferation. LY2603618 also significantly increased p38 and c-Jun N-terminal kinase (JNK) phosphorylation. Pretreatment with the JNK inhibitor reduced cleavage of caspase-3 and PARP levels in LY2603618-treated cells. These results suggest the following: (i) the biological consequences of LY2603618 in lung cancer cells is associated with both inhibition of Chk1 phosphorylation on S296 and activation of the DNA damage response network; and (ii) the anticancer property of LY2603618 might be increased by inhibiting autophagy. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Feng-Ze</ForeName><Initials>FZ</Initials><AffiliationInfo><Affiliation>School of Biological Science, Taishan Medical University, Taian, 271016, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fei</LastName><ForeName>Hong-rong</ForeName><Initials>HR</Initials></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Ying-Jie</ForeName><Initials>YJ</Initials></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Ying-Kun</ForeName><Initials>YK</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Zhao-Mei</ForeName><Initials>ZM</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xue-Ying</ForeName><Initials>XY</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Xiao-Yi</ForeName><Initials>XY</Initials></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Ji-Guo</ForeName><Initials>JG</Initials></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Bao-Liang</ForeName><Initials>BL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Apoptosis</MedlineTA><NlmUniqueID>9712129</NlmUniqueID><ISSNLinking>1360-8185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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