Phosphorylated heat shock protein 27 as a potential biomarker to predict the role of chemotherapy-induced autophagy in osteosarcoma response to therapy.
Identifieur interne : 000093 ( PubMed/Checkpoint ); précédent : 000092; suivant : 000094Phosphorylated heat shock protein 27 as a potential biomarker to predict the role of chemotherapy-induced autophagy in osteosarcoma response to therapy.
Auteurs : Janice M. Santiago-O'Farrill [États-Unis] ; Eugenie S. Kleinerman [États-Unis] ; Mario G. Hollomon [États-Unis] ; Andrew Livingston [États-Unis] ; Wei-Lien Wang [États-Unis] ; Jen-Wei Tsai [États-Unis] ; Nancy B. Gordon [États-Unis]Source :
- Oncotarget [ 1949-2553 ] ; 2018.
Abstract
Autophagy is a catabolic process involved in cellular homeostasis. Autophagy is increased above homeostatic levels by chemotherapy, and this can either promote or inhibit tumor growth. We previously demonstrated that aerosol gemcitabine (GCB) has a therapeutic effect against osteosarcoma (OS) lung metastases. However, some tumor cells failed to respond to the treatment and persisted as isolated lung metastasis. Here, we examined the mechanisms underlying the dual role of chemotherapy-induced autophagy in OS and sought to identify biomarkers to predict OS response to treatment. In this study, we demonstrate that treatment of various OS cells with GCB induced autophagy. We also showed that GCB reduces the phosphorylation of AKT, mTOR and p70S6K and that GCB-induced autophagy in OS can lead to either cell survival or cell death. Blocking autophagy enhanced the sensitivity of LM7 OS cells and decreased the sensitivity of CCH-OS-D and K7M3 OS cells to GCB. Using a kinase array, we also demonstrated that differences in the phosphorylated heat shock protein 27 (p-HSP27) expression in the various OS cell lines after treatment with GCB, correlates to whether chemotherapy-induced autophagy will lead to increase or decrease OS cells sensitivity to therapy. Increased p-HSP27 was associated with increased sensitivity to anticancer drug treatment when autophagy is inhibited. The results of this study reveal a dual role of autophagy in OS cells sensitivity to chemotherapy and suggest that p-HSP27 could represent a predictive biomarker of whether combination therapy with autophagy modulators and chemotherapeutic drugs will be beneficial for OS patients.
DOI: 10.18632/oncotarget.20308
PubMed: 29416717
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Santiago-O'Farrill</name><affiliation wicri:level="2"><nlm:affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Kleinerman, Eugenie S" sort="Kleinerman, Eugenie S" uniqKey="Kleinerman E" first="Eugenie S" last="Kleinerman">Eugenie S. Kleinerman</name><affiliation wicri:level="2"><nlm:affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Hollomon, Mario G" sort="Hollomon, Mario G" uniqKey="Hollomon M" first="Mario G" last="Hollomon">Mario G. Hollomon</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology, Texas Southern University, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biology, Texas Southern University, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Livingston, Andrew" sort="Livingston, Andrew" uniqKey="Livingston A" first="Andrew" last="Livingston">Andrew Livingston</name><affiliation wicri:level="2"><nlm:affiliation>Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Wang, Wei Lien" sort="Wang, Wei Lien" uniqKey="Wang W" first="Wei-Lien" last="Wang">Wei-Lien Wang</name><affiliation wicri:level="2"><nlm:affiliation>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Tsai, Jen Wei" sort="Tsai, Jen Wei" uniqKey="Tsai J" first="Jen-Wei" last="Tsai">Jen-Wei Tsai</name><affiliation wicri:level="2"><nlm:affiliation>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author><author><name sortKey="Gordon, Nancy B" sort="Gordon, Nancy B" uniqKey="Gordon N" first="Nancy B" last="Gordon">Nancy B. Gordon</name><affiliation wicri:level="2"><nlm:affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas</wicri:regionArea><placeName><region type="state">Texas</region></placeName></affiliation></author></analytic><series><title level="j">Oncotarget</title><idno type="eISSN">1949-2553</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is a catabolic process involved in cellular homeostasis. Autophagy is increased above homeostatic levels by chemotherapy, and this can either promote or inhibit tumor growth. We previously demonstrated that aerosol gemcitabine (GCB) has a therapeutic effect against osteosarcoma (OS) lung metastases. However, some tumor cells failed to respond to the treatment and persisted as isolated lung metastasis. Here, we examined the mechanisms underlying the dual role of chemotherapy-induced autophagy in OS and sought to identify biomarkers to predict OS response to treatment. In this study, we demonstrate that treatment of various OS cells with GCB induced autophagy. We also showed that GCB reduces the phosphorylation of AKT, mTOR and p70S6K and that GCB-induced autophagy in OS can lead to either cell survival or cell death. Blocking autophagy enhanced the sensitivity of LM7 OS cells and decreased the sensitivity of CCH-OS-D and K7M3 OS cells to GCB. Using a kinase array, we also demonstrated that differences in the phosphorylated heat shock protein 27 (p-HSP27) expression in the various OS cell lines after treatment with GCB, correlates to whether chemotherapy-induced autophagy will lead to increase or decrease OS cells sensitivity to therapy. Increased p-HSP27 was associated with increased sensitivity to anticancer drug treatment when autophagy is inhibited. The results of this study reveal a dual role of autophagy in OS cells sensitivity to chemotherapy and suggest that p-HSP27 could represent a predictive biomarker of whether combination therapy with autophagy modulators and chemotherapeutic drugs will be beneficial for OS patients.</div></front></TEI><pubmed><MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM"><PMID Version="1">29416717</PMID><DateRevised><Year>2019</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>2</Issue><PubDate><Year>2018</Year><Month>Jan</Month><Day>05</Day></PubDate></JournalIssue><Title>Oncotarget</Title><ISOAbbreviation>Oncotarget</ISOAbbreviation></Journal><ArticleTitle>Phosphorylated heat shock protein 27 as a potential biomarker to predict the role of chemotherapy-induced autophagy in osteosarcoma response to therapy.</ArticleTitle><Pagination><MedlinePgn>1602-1616</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.20308</ELocationID><Abstract><AbstractText>Autophagy is a catabolic process involved in cellular homeostasis. Autophagy is increased above homeostatic levels by chemotherapy, and this can either promote or inhibit tumor growth. We previously demonstrated that aerosol gemcitabine (GCB) has a therapeutic effect against osteosarcoma (OS) lung metastases. However, some tumor cells failed to respond to the treatment and persisted as isolated lung metastasis. Here, we examined the mechanisms underlying the dual role of chemotherapy-induced autophagy in OS and sought to identify biomarkers to predict OS response to treatment. In this study, we demonstrate that treatment of various OS cells with GCB induced autophagy. We also showed that GCB reduces the phosphorylation of AKT, mTOR and p70S6K and that GCB-induced autophagy in OS can lead to either cell survival or cell death. Blocking autophagy enhanced the sensitivity of LM7 OS cells and decreased the sensitivity of CCH-OS-D and K7M3 OS cells to GCB. Using a kinase array, we also demonstrated that differences in the phosphorylated heat shock protein 27 (p-HSP27) expression in the various OS cell lines after treatment with GCB, correlates to whether chemotherapy-induced autophagy will lead to increase or decrease OS cells sensitivity to therapy. Increased p-HSP27 was associated with increased sensitivity to anticancer drug treatment when autophagy is inhibited. The results of this study reveal a dual role of autophagy in OS cells sensitivity to chemotherapy and suggest that p-HSP27 could represent a predictive biomarker of whether combination therapy with autophagy modulators and chemotherapeutic drugs will be beneficial for OS patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Santiago-O'Farrill</LastName><ForeName>Janice M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kleinerman</LastName><ForeName>Eugenie S</ForeName><Initials>ES</Initials><AffiliationInfo><Affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hollomon</LastName><ForeName>Mario G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Department of Biology, Texas Southern University, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Livingston</LastName><ForeName>Andrew</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Wei-Lien</ForeName><Initials>WL</Initials><AffiliationInfo><Affiliation>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsai</LastName><ForeName>Jen-Wei</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gordon</LastName><ForeName>Nancy B</ForeName><Initials>NB</Initials><AffiliationInfo><Affiliation>Division of Pediatrics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K12 CA088084</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>08</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Oncotarget</MedlineTA><NlmUniqueID>101532965</NlmUniqueID><ISSNLinking>1949-2553</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Beclin</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">gemcitabine</Keyword><Keyword MajorTopicYN="N">hydroxychloroquine</Keyword><Keyword MajorTopicYN="N">osteosarcoma</Keyword></KeywordList><CoiStatement>CONFLICTS OF INTEREST There are no conflicts of interest to disclose.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>10</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>05</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2018</Year><Month>2</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>2</Month><Day>9</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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