Prognostic and therapeutic potential of Adenylate kinase 2 in lung adenocarcinoma.
Identifieur interne : 000020 ( PubMed/Corpus ); précédent : 000019; suivant : 000021Prognostic and therapeutic potential of Adenylate kinase 2 in lung adenocarcinoma.
Auteurs : Huibin Liu ; Yan Pu ; Quhai Amina ; Qiang Wang ; Mengmeng Zhang ; Jianzhong Song ; Jun Guo ; Mahmut MardanSource :
- Scientific reports [ 2045-2322 ] ; 2019.
Abstract
Adenylate kinase 2 (AK2), an isoenzyme of the AK family, may have momentous extra-mitochondrial functions, especially in tumourigenesis in addition to the well-known control of energy metabolism. In this study, we provided the first evidence that AK2 is overexpressed in lung adenocarcinoma. The positive expression of AK2 is associated with tumor progression, and poor survival in patients with pulmonary adenocarcinoma. Knockdown of AK2 could suppress proliferation, migration, and invasion as well as induce apoptosis and autophagy in human lung adenocarcinoma cells. Remarkably, silencing AK2 exerted the greater tumor suppression roles when combined with hydroxychloroquine, an effective autophagy inhibitor, in vitro and in xenografts mouse models. Our data have probably provided preclinical proof that systematic inhibition of AK2 and autophagy could be therapeutically effective on lung cancer.
DOI: 10.1038/s41598-019-53594-4
PubMed: 31780678
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Prognostic and therapeutic potential of Adenylate kinase 2 in lung adenocarcinoma.</title><author><name sortKey="Liu, Huibin" sort="Liu, Huibin" uniqKey="Liu H" first="Huibin" last="Liu">Huibin Liu</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China. 1047893820@qq.com.</nlm:affiliation></affiliation></author><author><name sortKey="Pu, Yan" sort="Pu, Yan" uniqKey="Pu Y" first="Yan" last="Pu">Yan Pu</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Amina, Quhai" sort="Amina, Quhai" uniqKey="Amina Q" first="Quhai" last="Amina">Quhai Amina</name><affiliation><nlm:affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Qiang" sort="Wang, Qiang" uniqKey="Wang Q" first="Qiang" last="Wang">Qiang Wang</name><affiliation><nlm:affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Mengmeng" sort="Zhang, Mengmeng" uniqKey="Zhang M" first="Mengmeng" last="Zhang">Mengmeng Zhang</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Jianzhong" sort="Song, Jianzhong" uniqKey="Song J" first="Jianzhong" last="Song">Jianzhong Song</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Guo, Jun" sort="Guo, Jun" uniqKey="Guo J" first="Jun" last="Guo">Jun Guo</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Mardan, Mahmut" sort="Mardan, Mahmut" uniqKey="Mardan M" first="Mahmut" last="Mardan">Mahmut Mardan</name><affiliation><nlm:affiliation>School of pharmacy, Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31780678</idno><idno type="pmid">31780678</idno><idno type="doi">10.1038/s41598-019-53594-4</idno><idno type="wicri:Area/PubMed/Corpus">000020</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000020</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Prognostic and therapeutic potential of Adenylate kinase 2 in lung adenocarcinoma.</title><author><name sortKey="Liu, Huibin" sort="Liu, Huibin" uniqKey="Liu H" first="Huibin" last="Liu">Huibin Liu</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China. 1047893820@qq.com.</nlm:affiliation></affiliation></author><author><name sortKey="Pu, Yan" sort="Pu, Yan" uniqKey="Pu Y" first="Yan" last="Pu">Yan Pu</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Amina, Quhai" sort="Amina, Quhai" uniqKey="Amina Q" first="Quhai" last="Amina">Quhai Amina</name><affiliation><nlm:affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Qiang" sort="Wang, Qiang" uniqKey="Wang Q" first="Qiang" last="Wang">Qiang Wang</name><affiliation><nlm:affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Mengmeng" sort="Zhang, Mengmeng" uniqKey="Zhang M" first="Mengmeng" last="Zhang">Mengmeng Zhang</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Song, Jianzhong" sort="Song, Jianzhong" uniqKey="Song J" first="Jianzhong" last="Song">Jianzhong Song</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Guo, Jun" sort="Guo, Jun" uniqKey="Guo J" first="Jun" last="Guo">Jun Guo</name><affiliation><nlm:affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author><author><name sortKey="Mardan, Mahmut" sort="Mardan, Mahmut" uniqKey="Mardan M" first="Mahmut" last="Mardan">Mahmut Mardan</name><affiliation><nlm:affiliation>School of pharmacy, Xinjiang Medical University, Urumqi, China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</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">Adenylate kinase 2 (AK2), an isoenzyme of the AK family, may have momentous extra-mitochondrial functions, especially in tumourigenesis in addition to the well-known control of energy metabolism. In this study, we provided the first evidence that AK2 is overexpressed in lung adenocarcinoma. The positive expression of AK2 is associated with tumor progression, and poor survival in patients with pulmonary adenocarcinoma. Knockdown of AK2 could suppress proliferation, migration, and invasion as well as induce apoptosis and autophagy in human lung adenocarcinoma cells. Remarkably, silencing AK2 exerted the greater tumor suppression roles when combined with hydroxychloroquine, an effective autophagy inhibitor, in vitro and in xenografts mouse models. Our data have probably provided preclinical proof that systematic inhibition of AK2 and autophagy could be therapeutically effective on lung cancer.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">31780678</PMID><DateRevised><Year>2020</Year><Month>01</Month><Day>08</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>Nov</Month><Day>28</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Prognostic and therapeutic potential of Adenylate kinase 2 in lung adenocarcinoma.</ArticleTitle><Pagination><MedlinePgn>17757</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-019-53594-4</ELocationID><Abstract><AbstractText>Adenylate kinase 2 (AK2), an isoenzyme of the AK family, may have momentous extra-mitochondrial functions, especially in tumourigenesis in addition to the well-known control of energy metabolism. In this study, we provided the first evidence that AK2 is overexpressed in lung adenocarcinoma. The positive expression of AK2 is associated with tumor progression, and poor survival in patients with pulmonary adenocarcinoma. Knockdown of AK2 could suppress proliferation, migration, and invasion as well as induce apoptosis and autophagy in human lung adenocarcinoma cells. Remarkably, silencing AK2 exerted the greater tumor suppression roles when combined with hydroxychloroquine, an effective autophagy inhibitor, in vitro and in xenografts mouse models. Our data have probably provided preclinical proof that systematic inhibition of AK2 and autophagy could be therapeutically effective on lung cancer.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Huibin</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China. 1047893820@qq.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pu</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-0673-6230</Identifier><AffiliationInfo><Affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Amina</LastName><ForeName>Quhai</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Qiang</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of pulmonary oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Mengmeng</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Jianzhong</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of cancer control, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, China.</Affiliation></AffiliationInfo></Author><Author 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