Enhancing therapeutic efficacy of the MEK inhibitor, MEK162, by blocking autophagy or inhibiting PI3K/Akt signaling in human lung cancer cells.
Identifieur interne : 000254 ( PubMed/Curation ); précédent : 000253; suivant : 000255Enhancing therapeutic efficacy of the MEK inhibitor, MEK162, by blocking autophagy or inhibiting PI3K/Akt signaling in human lung cancer cells.
Auteurs : Weilong Yao [États-Unis] ; Ping Yue [États-Unis] ; Guojing Zhang [États-Unis] ; Taofeek K. Owonikoko [États-Unis] ; Fadlo R. Khuri [États-Unis] ; Shi-Yong Sun [États-Unis]Source :
- Cancer letters [ 1872-7980 ] ; 2015.
Descripteurs français
- KwdFr :
- Autophagie (), Benzimidazoles (pharmacologie), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (enzymologie), Humains, Lignée cellulaire tumorale, MAP Kinase Kinase Kinases (antagonistes et inhibiteurs), Phosphatidylinositol 3-kinases (métabolisme), Protéines proto-oncogènes c-akt (métabolisme), Transduction du signal (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (enzymologie).
- MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- antagonistes et inhibiteurs : MAP Kinase Kinase Kinases.
- enzymologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- métabolisme : Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt.
- pharmacologie : Benzimidazoles.
- Autophagie, Humains, Lignée cellulaire tumorale, Transduction du signal.
English descriptors
- KwdEn :
- Autophagy (drug effects), Benzimidazoles (pharmacology), Carcinoma, Non-Small-Cell Lung (enzymology), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Humans, Lung Neoplasms (enzymology), Lung Neoplasms (pathology), MAP Kinase Kinase Kinases (antagonists & inhibitors), Phosphatidylinositol 3-Kinases (metabolism), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , antagonists & inhibitors : MAP Kinase Kinase Kinases.
- chemical , metabolism : Proto-Oncogene Proteins c-akt.
- chemical , pharmacology : Benzimidazoles.
- drug effects : Autophagy, Signal Transduction.
- enzymology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- metabolism : Phosphatidylinositol 3-Kinases.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- Cell Line, Tumor, Humans.
Abstract
Human non-small cell lung cancer (NSCLC) displays activated MEK/ERK signaling due to a high frequency of K-Ras mutation and is thus a potential candidate for MEK-targeted therapy. The current study focuses on demonstrating the activity of MEK162 (binimetinib), a MEK inhibitor under clinical testing, against NSCLC and exploring possible mechanism-driven strategies to enhance its therapeutic efficacy. MEK162 inhibits the growth of human NSCLC cell lines with varied potencies through induction of G1 cell cycle arrest and apoptosis. Moreover, it induces autophagy and accordingly the combination of MEK162 with the autophagy inhibitor, chloroquine, synergistically inhibits the growth of NSCLC cells and enhances apoptosis. MEK162 activates Akt signaling while effectively inhibiting MEK/ERK signaling. Accordingly, the combination of MEK162 and BKM120 (buparlisib), a pan-PI3K inhibitor, abrogates induced Akt activation and significantly augments therapeutic efficacy against the growth of NSCLC cells both in vitro and in vivo. Hence our findings warrant further evaluation of these rational combinations in the clinic.
DOI: 10.1016/j.canlet.2015.04.028
PubMed: 25937299
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The current study focuses on demonstrating the activity of MEK162 (binimetinib), a MEK inhibitor under clinical testing, against NSCLC and exploring possible mechanism-driven strategies to enhance its therapeutic efficacy. MEK162 inhibits the growth of human NSCLC cell lines with varied potencies through induction of G1 cell cycle arrest and apoptosis. Moreover, it induces autophagy and accordingly the combination of MEK162 with the autophagy inhibitor, chloroquine, synergistically inhibits the growth of NSCLC cells and enhances apoptosis. MEK162 activates Akt signaling while effectively inhibiting MEK/ERK signaling. Accordingly, the combination of MEK162 and BKM120 (buparlisib), a pan-PI3K inhibitor, abrogates induced Akt activation and significantly augments therapeutic efficacy against the growth of NSCLC cells both in vitro and in vivo. Hence our findings warrant further evaluation of these rational combinations in the clinic. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25937299</PMID><DateCompleted><Year>2015</Year><Month>08</Month><Day>06</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7980</ISSN><JournalIssue CitedMedium="Internet"><Volume>364</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Aug</Month><Day>01</Day></PubDate></JournalIssue><Title>Cancer letters</Title><ISOAbbreviation>Cancer Lett.</ISOAbbreviation></Journal><ArticleTitle>Enhancing therapeutic efficacy of the MEK inhibitor, MEK162, by blocking autophagy or inhibiting PI3K/Akt signaling in human lung cancer cells.</ArticleTitle><Pagination><MedlinePgn>70-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.canlet.2015.04.028</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0304-3835(15)00307-9</ELocationID><Abstract><AbstractText>Human non-small cell lung cancer (NSCLC) displays activated MEK/ERK signaling due to a high frequency of K-Ras mutation and is thus a potential candidate for MEK-targeted therapy. The current study focuses on demonstrating the activity of MEK162 (binimetinib), a MEK inhibitor under clinical testing, against NSCLC and exploring possible mechanism-driven strategies to enhance its therapeutic efficacy. MEK162 inhibits the growth of human NSCLC cell lines with varied potencies through induction of G1 cell cycle arrest and apoptosis. Moreover, it induces autophagy and accordingly the combination of MEK162 with the autophagy inhibitor, chloroquine, synergistically inhibits the growth of NSCLC cells and enhances apoptosis. MEK162 activates Akt signaling while effectively inhibiting MEK/ERK signaling. Accordingly, the combination of MEK162 and BKM120 (buparlisib), a pan-PI3K inhibitor, abrogates induced Akt activation and significantly augments therapeutic efficacy against the growth of NSCLC cells both in vitro and in vivo. Hence our findings warrant further evaluation of these rational combinations in the clinic. </AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yao</LastName><ForeName>Weilong</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Respiration, Xiangya Hospital and Xiangya School of Medicine, Central South University, Changsha, Hunan, China; Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yue</LastName><ForeName>Ping</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Guojing</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Owonikoko</LastName><ForeName>Taofeek K</ForeName><Initials>TK</Initials><AffiliationInfo><Affiliation>Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khuri</LastName><ForeName>Fadlo R</ForeName><Initials>FR</Initials><AffiliationInfo><Affiliation>Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sun</LastName><ForeName>Shi-Yong</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Department of Hematology and Medical Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA. Electronic address: ssun@emory.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA118450</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA160522</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>04</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Cancer Lett</MedlineTA><NlmUniqueID>7600053</NlmUniqueID><ISSNLinking>0304-3835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001562">Benzimidazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>181R97MR71</RegistryNumber><NameOfSubstance UI="C581313">binimetinib</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.25</RegistryNumber><NameOfSubstance UI="D020930">MAP Kinase Kinase Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001562" MajorTopicYN="N">Benzimidazoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020930" MajorTopicYN="N">MAP Kinase Kinase Kinases</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autophagy</Keyword><Keyword MajorTopicYN="N">BKM120</Keyword><Keyword MajorTopicYN="N">Lung cancer</Keyword><Keyword MajorTopicYN="N">MEK162</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>03</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>04</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>04</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>8</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25937299</ArticleId><ArticleId IdType="pii">S0304-3835(15)00307-9</ArticleId><ArticleId IdType="doi">10.1016/j.canlet.2015.04.028</ArticleId><ArticleId IdType="pmc">PMC4450809</ArticleId><ArticleId IdType="mid">NIHMS689126</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Oncogene. 1999 Apr 8;18(14):2357-65</Citation><ArticleIdList><ArticleId IdType="pubmed">10327056</ArticleId></ArticleIdList></Reference><Reference><Citation>Lung Cancer. 2014 Nov;86(2):121-5</Citation><ArticleIdList><ArticleId IdType="pubmed">25257766</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Biol Ther. 2004 Nov;3(11):1092-8; discussion 1099-1101</Citation><ArticleIdList><ArticleId IdType="pubmed">15467440</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2007 May 11;282(19):14056-64</Citation><ArticleIdList><ArticleId IdType="pubmed">17360704</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2008 Jan 11;132(1):27-42</Citation><ArticleIdList><ArticleId IdType="pubmed">18191218</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Biol Ther. 2008 Dec;7(12):1952-8</Citation><ArticleIdList><ArticleId IdType="pubmed">18981735</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cancer Ther. 2009 Apr;8(4):834-43</Citation><ArticleIdList><ArticleId IdType="pubmed">19372556</ArticleId></ArticleIdList></Reference><Reference><Citation>Int J Cancer. 2009 Nov 15;125(10):2332-41</Citation><ArticleIdList><ArticleId IdType="pubmed">19637312</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cancer Ther. 2010 Jul;9(7):1985-94</Citation><ArticleIdList><ArticleId IdType="pubmed">20587667</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Res. 2010 Nov 1;70(21):8736-47</Citation><ArticleIdList><ArticleId IdType="pubmed">20959481</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Biochem Sci. 2011 Jun;36(6):320-8</Citation><ArticleIdList><ArticleId IdType="pubmed">21531565</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Clin Oncol. 2011 Sep;8(9):528-39</Citation><ArticleIdList><ArticleId IdType="pubmed">21587219</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Discov. 2015 Mar;5(3):304-15</Citation><ArticleIdList><ArticleId IdType="pubmed">25572173</ArticleId></ArticleIdList></Reference><Reference><Citation>Tumour Biol. 2015 Jul;36(7):5699-706</Citation><ArticleIdList><ArticleId IdType="pubmed">25697899</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Res. 1997 Nov 1;57(21):4931-9</Citation><ArticleIdList><ArticleId IdType="pubmed">9354460</ArticleId></ArticleIdList></Reference><Reference><Citation>J Cell Physiol. 1997 Nov;173(2):279-84</Citation><ArticleIdList><ArticleId IdType="pubmed">9365537</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Biol Ther. 2011 Sep 15;12(6):549-55</Citation><ArticleIdList><ArticleId IdType="pubmed">21738008</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Res. 2012 Jul 1;72(13):3228-37</Citation><ArticleIdList><ArticleId IdType="pubmed">22552284</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Lett. 2012 Dec 28;325(2):139-46</Citation><ArticleIdList><ArticleId IdType="pubmed">22781393</ArticleId></ArticleIdList></Reference><Reference><Citation>PLoS One. 2012;7(8):e44146</Citation><ArticleIdList><ArticleId IdType="pubmed">22952903</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Oncol. 2013 Jan;14(1):38-47</Citation><ArticleIdList><ArticleId IdType="pubmed">23200175</ArticleId></ArticleIdList></Reference><Reference><Citation>Lancet Oncol. 2013 Mar;14(3):249-56</Citation><ArticleIdList><ArticleId IdType="pubmed">23414587</ArticleId></ArticleIdList></Reference><Reference><Citation>Sci Transl Med. 2013 Jul 31;5(196):196ra98</Citation><ArticleIdList><ArticleId IdType="pubmed">23903755</ArticleId></ArticleIdList></Reference><Reference><Citation>Expert Opin Investig Drugs. 2014 Mar;23(3):295-304</Citation><ArticleIdList><ArticleId IdType="pubmed">24387133</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cancer. 2014;13:45</Citation><ArticleIdList><ArticleId IdType="pubmed">24588908</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncogene. 2014 Sep 25;33(39):4724-34</Citation><ArticleIdList><ArticleId IdType="pubmed">24141786</ArticleId></ArticleIdList></Reference><Reference><Citation>Br J Cancer. 2014 Oct 28;111(9):1788-801</Citation><ArticleIdList><ArticleId IdType="pubmed">25167228</ArticleId></ArticleIdList></Reference><Reference><Citation>Blood. 2014 Nov 27;124(23):3420-30</Citation><ArticleIdList><ArticleId IdType="pubmed">25253770</ArticleId></ArticleIdList></Reference><Reference><Citation>J Natl Cancer Inst. 2004 Dec 1;96(23):1769-80</Citation><ArticleIdList><ArticleId IdType="pubmed">15572759</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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