Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy.
Identifieur interne : 000116 ( PubMed/Corpus ); précédent : 000115; suivant : 000117Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy.
Auteurs : Mija Marinkovi ; Matilda Šprung ; Maja Buljubaši ; Ivana NovakSource :
- Oxidative medicine and cellular longevity [ 1942-0994 ] ; 2018.
English descriptors
- KwdEn :
- MESH :
Abstract
In the last two decades, accumulating evidence pointed to the importance of autophagy in various human diseases. As an essential evolutionary catabolic process of cytoplasmatic component digestion, it is generally believed that modulating autophagic activity, through targeting specific regulatory actors in the core autophagy machinery, may impact disease processes. Both autophagy upregulation and downregulation have been found in cancers, suggesting its dual oncogenic and tumor suppressor properties during malignant transformation. Identification of the key autophagy targets is essential for the development of new therapeutic agents. Despite this great potential, no therapies are currently available that specifically focus on autophagy modulation. Although drugs like rapamycin, chloroquine, hydroxychloroquine, and others act as autophagy modulators, they were not originally developed for this purpose. Thus, autophagy may represent a new and promising pharmacologic target for future drug development and therapeutic applications in human diseases. Here, we summarize our current knowledge in regard to the interplay between autophagy and malignancy in the most significant tumor types: pancreatic, breast, hepatocellular, colorectal, and lung cancer, which have been studied in respect to autophagy manipulation as a promising therapeutic strategy. Finally, we present an overview of the most recent advances in therapeutic strategies involving autophagy modulators in cancer.
DOI: 10.1155/2018/8023821
PubMed: 29643976
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pubmed:29643976Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy.</title><author><name sortKey="Marinkovi, Mija" sort="Marinkovi, Mija" uniqKey="Marinkovi M" first="Mija" last="Marinkovi">Mija Marinkovi</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Sprung, Matilda" sort="Sprung, Matilda" uniqKey="Sprung M" first="Matilda" last="Šprung">Matilda Šprung</name><affiliation><nlm:affiliation>Faculty of Science, University of Split, Ruđera Boškovića 33, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Buljubasi, Maja" sort="Buljubasi, Maja" uniqKey="Buljubasi M" first="Maja" last="Buljubaši">Maja Buljubaši</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Novak, Ivana" sort="Novak, Ivana" uniqKey="Novak I" first="Ivana" last="Novak">Ivana Novak</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29643976</idno><idno type="pmid">29643976</idno><idno type="doi">10.1155/2018/8023821</idno><idno type="wicri:Area/PubMed/Corpus">000116</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000116</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy.</title><author><name sortKey="Marinkovi, Mija" sort="Marinkovi, Mija" uniqKey="Marinkovi M" first="Mija" last="Marinkovi">Mija Marinkovi</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Sprung, Matilda" sort="Sprung, Matilda" uniqKey="Sprung M" first="Matilda" last="Šprung">Matilda Šprung</name><affiliation><nlm:affiliation>Faculty of Science, University of Split, Ruđera Boškovića 33, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Buljubasi, Maja" sort="Buljubasi, Maja" uniqKey="Buljubasi M" first="Maja" last="Buljubaši">Maja Buljubaši</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author><author><name sortKey="Novak, Ivana" sort="Novak, Ivana" uniqKey="Novak I" first="Ivana" last="Novak">Ivana Novak</name><affiliation><nlm:affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Oxidative medicine and cellular longevity</title><idno type="eISSN">1942-0994</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autophagy (physiology)</term><term>Humans</term><term>Neoplasms (pathology)</term><term>Neoplasms (therapy)</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the last two decades, accumulating evidence pointed to the importance of autophagy in various human diseases. As an essential evolutionary catabolic process of cytoplasmatic component digestion, it is generally believed that modulating autophagic activity, through targeting specific regulatory actors in the core autophagy machinery, may impact disease processes. Both autophagy upregulation and downregulation have been found in cancers, suggesting its dual oncogenic and tumor suppressor properties during malignant transformation. Identification of the key autophagy targets is essential for the development of new therapeutic agents. Despite this great potential, no therapies are currently available that specifically focus on autophagy modulation. Although drugs like rapamycin, chloroquine, hydroxychloroquine, and others act as autophagy modulators, they were not originally developed for this purpose. Thus, autophagy may represent a new and promising pharmacologic target for future drug development and therapeutic applications in human diseases. Here, we summarize our current knowledge in regard to the interplay between autophagy and malignancy in the most significant tumor types: pancreatic, breast, hepatocellular, colorectal, and lung cancer, which have been studied in respect to autophagy manipulation as a promising therapeutic strategy. Finally, we present an overview of the most recent advances in therapeutic strategies involving autophagy modulators in cancer.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29643976</PMID><DateCompleted><Year>2018</Year><Month>09</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>14</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1942-0994</ISSN><JournalIssue CitedMedium="Internet"><Volume>2018</Volume><PubDate><Year>2018</Year></PubDate></JournalIssue><Title>Oxidative medicine and cellular longevity</Title><ISOAbbreviation>Oxid Med Cell Longev</ISOAbbreviation></Journal><ArticleTitle>Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy.</ArticleTitle><Pagination><MedlinePgn>8023821</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1155/2018/8023821</ELocationID><Abstract><AbstractText>In the last two decades, accumulating evidence pointed to the importance of autophagy in various human diseases. As an essential evolutionary catabolic process of cytoplasmatic component digestion, it is generally believed that modulating autophagic activity, through targeting specific regulatory actors in the core autophagy machinery, may impact disease processes. Both autophagy upregulation and downregulation have been found in cancers, suggesting its dual oncogenic and tumor suppressor properties during malignant transformation. Identification of the key autophagy targets is essential for the development of new therapeutic agents. Despite this great potential, no therapies are currently available that specifically focus on autophagy modulation. Although drugs like rapamycin, chloroquine, hydroxychloroquine, and others act as autophagy modulators, they were not originally developed for this purpose. Thus, autophagy may represent a new and promising pharmacologic target for future drug development and therapeutic applications in human diseases. Here, we summarize our current knowledge in regard to the interplay between autophagy and malignancy in the most significant tumor types: pancreatic, breast, hepatocellular, colorectal, and lung cancer, which have been studied in respect to autophagy manipulation as a promising therapeutic strategy. Finally, we present an overview of the most recent advances in therapeutic strategies involving autophagy modulators in cancer.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Marinković</LastName><ForeName>Mija</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Šprung</LastName><ForeName>Matilda</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Faculty of Science, University of Split, Ruđera Boškovića 33, 21000 Split, Croatia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buljubašić</LastName><ForeName>Maja</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Novak</LastName><ForeName>Ivana</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0003-0682-7052</Identifier><AffiliationInfo><Affiliation>School of Medicine, University of Split, Šoltanska 2, 21000 Split, Croatia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Oxid Med Cell Longev</MedlineTA><NlmUniqueID>101479826</NlmUniqueID><ISSNLinking>1942-0994</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" 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