Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation
Objective This study aimed to investigate the regulatory effect of ivermectin (IVM) on energy metabolism in glioma progression, and provide a reference for the treatment of glioma. Methods Glioma cells were treated with IVM to measure cell viability, autophagy marker protein expression, ATP content,...
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Veröffentlicht in: | Environmental toxicology 2022-04, Vol.37 (4), p.754-764 |
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description | Objective
This study aimed to investigate the regulatory effect of ivermectin (IVM) on energy metabolism in glioma progression, and provide a reference for the treatment of glioma.
Methods
Glioma cells were treated with IVM to measure cell viability, autophagy marker protein expression, ATP content, glucose uptake, pyruvate content, and expression of key enzymes of glycolysis. Glucose transporter 4 (GLUT4) or siGLUT4 was transfected in IVM treated U87 cells to investigate the effect of GLUT4 on cellular glycolysis and autophagy. The JAK2 inhibitor AZD‐1480 was introduced to explore the specific mechanism by which IVM regulates glycolysis and autophagy. Rat models of glioma xenograft were constructed and treated with 10 mg/kg IVM to observe tumor growth and examine the expression levels of GLUT4 and autophagy marker proteins in tumor tissues.
Results
IVM inhibited glioma cell survival and promoted cell death. IVM promoted LC3‐II protein expression and inhibited p62/SQSTM1 protein expression in glioma cells. IVM decreased adenosine‐triphosphate (ATP) and pyruvate content, promoted glucose uptake, and reduced HK2 and PFK1 protein expression in U87 cells. IVM inhibited GLUT4 protein expression, and overexpression of GLUT4 promoted glycolysis and inhibited autophagic cell death in U87 cells. IVM inhibited glycolysis by blocking GLUT4 mediated the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activation. IVM inhibited tumor growth in vivo, decreased the protein expression of GLUT4, JAK2, HK2, and PFK1 in tumor tissues, decreased the phosphorylation levels of STAT3/STAT5, and promoted the expression of autophagy marker proteins.
Conclusions
IVM accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation. |
doi_str_mv | 10.1002/tox.23440 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2610082844</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2634412361</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3530-2465bedf20a206021d130a3df05732b22620465b53e27f47c43cb28d5215175e3</originalsourceid><addsrcrecordid>eNp1kc1u1TAQhS0Eoj-w4AWQJTZ0kd7x2Pnp8qqCUrhSF6QSu8hxnMQliS-205IX4XlxegsLJFYeab45njmHkDcMzhkAboL9eY5cCHhGjlmKmOSYF88fa0gEFOyInHh_BwAXWZq9JEdcXIDIc3FMfl3fazdqFcxEpVJ60E4G7amcg933sjOKNlqGntqWdoOxo6QRGjytF2qm3tQmTnaxtSg7LN54Gnpn566n9WDV97V3tbstBR11Y6JyQz9vv2y-ltuSetNNcliJffzgQS5xgWDuZTB2ekVetHLw-vXTe0puP34oLz8lu5ur68vtLlE85ZCgyNJaNy2CRMgAWcM4SN60kOYca8QMYUVSrjFvRa4EVzUWTYosZXmq-Sl5f9DdO_tj1j5Uo_HrgXLSdvYVZtHgAgshIvruH_TOzi5esFLRfIY8Y5E6O1DKWe-dbqu9M6N0S8WgWsOqYljVY1iRffukONfRnr_kn3QisDkAD2bQy_-VqvLm20HyN461nok</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2634412361</pqid></control><display><type>article</type><title>Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation</title><source>MEDLINE</source><source>Wiley Online Library</source><creator>Feng, Yi ; Wang, Jubo ; Cai, Bing ; Bai, Ximin ; Zhu, Yiru</creator><creatorcontrib>Feng, Yi ; Wang, Jubo ; Cai, Bing ; Bai, Ximin ; Zhu, Yiru</creatorcontrib><description>Objective
This study aimed to investigate the regulatory effect of ivermectin (IVM) on energy metabolism in glioma progression, and provide a reference for the treatment of glioma.
Methods
Glioma cells were treated with IVM to measure cell viability, autophagy marker protein expression, ATP content, glucose uptake, pyruvate content, and expression of key enzymes of glycolysis. Glucose transporter 4 (GLUT4) or siGLUT4 was transfected in IVM treated U87 cells to investigate the effect of GLUT4 on cellular glycolysis and autophagy. The JAK2 inhibitor AZD‐1480 was introduced to explore the specific mechanism by which IVM regulates glycolysis and autophagy. Rat models of glioma xenograft were constructed and treated with 10 mg/kg IVM to observe tumor growth and examine the expression levels of GLUT4 and autophagy marker proteins in tumor tissues.
Results
IVM inhibited glioma cell survival and promoted cell death. IVM promoted LC3‐II protein expression and inhibited p62/SQSTM1 protein expression in glioma cells. IVM decreased adenosine‐triphosphate (ATP) and pyruvate content, promoted glucose uptake, and reduced HK2 and PFK1 protein expression in U87 cells. IVM inhibited GLUT4 protein expression, and overexpression of GLUT4 promoted glycolysis and inhibited autophagic cell death in U87 cells. IVM inhibited glycolysis by blocking GLUT4 mediated the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activation. IVM inhibited tumor growth in vivo, decreased the protein expression of GLUT4, JAK2, HK2, and PFK1 in tumor tissues, decreased the phosphorylation levels of STAT3/STAT5, and promoted the expression of autophagy marker proteins.
Conclusions
IVM accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.23440</identifier><identifier>PMID: 34904774</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Adenosine ; Adenosine triphosphate ; Animal models ; Animals ; Apoptosis ; ATP ; Autophagic Cell Death - drug effects ; Autophagy ; Brain tumors ; Cell death ; Cell Line, Tumor ; Cell survival ; Cell viability ; Energy metabolism ; Glioma ; Glioma - metabolism ; Glioma cells ; Glucose ; Glucose transporter ; Glucose Transporter Type 4 - antagonists & inhibitors ; GLUT4 ; Glycolysis ; Humans ; Ivermectin ; Ivermectin - pharmacology ; Ivermectin - therapeutic use ; Janus kinase ; Janus kinase 2 ; Janus Kinases - metabolism ; Kinases ; Markers ; Metabolism ; Mortality ; Neoplasms ; Phosphorylation ; Protein expression ; Proteins ; Pyruvic acid ; Rats ; Signal Transduction ; Signaling ; STAT Transcription Factors - metabolism ; Stat3 protein ; Stat5 protein ; Survival ; the JAK/STAT signaling pathway ; Tissue ; Transcription ; Transducers ; Tumors ; Uptake ; Xenografts ; Xenotransplantation</subject><ispartof>Environmental toxicology, 2022-04, Vol.37 (4), p.754-764</ispartof><rights>2021 Wiley Periodicals LLC.</rights><rights>2022 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-2465bedf20a206021d130a3df05732b22620465b53e27f47c43cb28d5215175e3</citedby><cites>FETCH-LOGICAL-c3530-2465bedf20a206021d130a3df05732b22620465b53e27f47c43cb28d5215175e3</cites><orcidid>0000-0001-5023-2422</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.23440$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.23440$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34904774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Feng, Yi</creatorcontrib><creatorcontrib>Wang, Jubo</creatorcontrib><creatorcontrib>Cai, Bing</creatorcontrib><creatorcontrib>Bai, Ximin</creatorcontrib><creatorcontrib>Zhu, Yiru</creatorcontrib><title>Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>Objective
This study aimed to investigate the regulatory effect of ivermectin (IVM) on energy metabolism in glioma progression, and provide a reference for the treatment of glioma.
Methods
Glioma cells were treated with IVM to measure cell viability, autophagy marker protein expression, ATP content, glucose uptake, pyruvate content, and expression of key enzymes of glycolysis. Glucose transporter 4 (GLUT4) or siGLUT4 was transfected in IVM treated U87 cells to investigate the effect of GLUT4 on cellular glycolysis and autophagy. The JAK2 inhibitor AZD‐1480 was introduced to explore the specific mechanism by which IVM regulates glycolysis and autophagy. Rat models of glioma xenograft were constructed and treated with 10 mg/kg IVM to observe tumor growth and examine the expression levels of GLUT4 and autophagy marker proteins in tumor tissues.
Results
IVM inhibited glioma cell survival and promoted cell death. IVM promoted LC3‐II protein expression and inhibited p62/SQSTM1 protein expression in glioma cells. IVM decreased adenosine‐triphosphate (ATP) and pyruvate content, promoted glucose uptake, and reduced HK2 and PFK1 protein expression in U87 cells. IVM inhibited GLUT4 protein expression, and overexpression of GLUT4 promoted glycolysis and inhibited autophagic cell death in U87 cells. IVM inhibited glycolysis by blocking GLUT4 mediated the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activation. IVM inhibited tumor growth in vivo, decreased the protein expression of GLUT4, JAK2, HK2, and PFK1 in tumor tissues, decreased the phosphorylation levels of STAT3/STAT5, and promoted the expression of autophagy marker proteins.
Conclusions
IVM accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation.</description><subject>Adenosine</subject><subject>Adenosine triphosphate</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>ATP</subject><subject>Autophagic Cell Death - drug effects</subject><subject>Autophagy</subject><subject>Brain tumors</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cell survival</subject><subject>Cell viability</subject><subject>Energy metabolism</subject><subject>Glioma</subject><subject>Glioma - metabolism</subject><subject>Glioma cells</subject><subject>Glucose</subject><subject>Glucose transporter</subject><subject>Glucose Transporter Type 4 - antagonists & inhibitors</subject><subject>GLUT4</subject><subject>Glycolysis</subject><subject>Humans</subject><subject>Ivermectin</subject><subject>Ivermectin - pharmacology</subject><subject>Ivermectin - therapeutic use</subject><subject>Janus kinase</subject><subject>Janus kinase 2</subject><subject>Janus Kinases - metabolism</subject><subject>Kinases</subject><subject>Markers</subject><subject>Metabolism</subject><subject>Mortality</subject><subject>Neoplasms</subject><subject>Phosphorylation</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Pyruvic acid</subject><subject>Rats</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Stat3 protein</subject><subject>Stat5 protein</subject><subject>Survival</subject><subject>the JAK/STAT signaling pathway</subject><subject>Tissue</subject><subject>Transcription</subject><subject>Transducers</subject><subject>Tumors</subject><subject>Uptake</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1TAQhS0Eoj-w4AWQJTZ0kd7x2Pnp8qqCUrhSF6QSu8hxnMQliS-205IX4XlxegsLJFYeab45njmHkDcMzhkAboL9eY5cCHhGjlmKmOSYF88fa0gEFOyInHh_BwAXWZq9JEdcXIDIc3FMfl3fazdqFcxEpVJ60E4G7amcg933sjOKNlqGntqWdoOxo6QRGjytF2qm3tQmTnaxtSg7LN54Gnpn566n9WDV97V3tbstBR11Y6JyQz9vv2y-ltuSetNNcliJffzgQS5xgWDuZTB2ekVetHLw-vXTe0puP34oLz8lu5ur68vtLlE85ZCgyNJaNy2CRMgAWcM4SN60kOYca8QMYUVSrjFvRa4EVzUWTYosZXmq-Sl5f9DdO_tj1j5Uo_HrgXLSdvYVZtHgAgshIvruH_TOzi5esFLRfIY8Y5E6O1DKWe-dbqu9M6N0S8WgWsOqYljVY1iRffukONfRnr_kn3QisDkAD2bQy_-VqvLm20HyN461nok</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Feng, Yi</creator><creator>Wang, Jubo</creator><creator>Cai, Bing</creator><creator>Bai, Ximin</creator><creator>Zhu, Yiru</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5023-2422</orcidid></search><sort><creationdate>202204</creationdate><title>Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation</title><author>Feng, Yi ; Wang, Jubo ; Cai, Bing ; Bai, Ximin ; Zhu, Yiru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-2465bedf20a206021d130a3df05732b22620465b53e27f47c43cb28d5215175e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenosine</topic><topic>Adenosine triphosphate</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>ATP</topic><topic>Autophagic Cell Death - drug effects</topic><topic>Autophagy</topic><topic>Brain tumors</topic><topic>Cell death</topic><topic>Cell Line, Tumor</topic><topic>Cell survival</topic><topic>Cell viability</topic><topic>Energy metabolism</topic><topic>Glioma</topic><topic>Glioma - metabolism</topic><topic>Glioma cells</topic><topic>Glucose</topic><topic>Glucose transporter</topic><topic>Glucose Transporter Type 4 - antagonists & inhibitors</topic><topic>GLUT4</topic><topic>Glycolysis</topic><topic>Humans</topic><topic>Ivermectin</topic><topic>Ivermectin - pharmacology</topic><topic>Ivermectin - therapeutic use</topic><topic>Janus kinase</topic><topic>Janus kinase 2</topic><topic>Janus Kinases - metabolism</topic><topic>Kinases</topic><topic>Markers</topic><topic>Metabolism</topic><topic>Mortality</topic><topic>Neoplasms</topic><topic>Phosphorylation</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Pyruvic acid</topic><topic>Rats</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Stat3 protein</topic><topic>Stat5 protein</topic><topic>Survival</topic><topic>the JAK/STAT signaling pathway</topic><topic>Tissue</topic><topic>Transcription</topic><topic>Transducers</topic><topic>Tumors</topic><topic>Uptake</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Feng, Yi</creatorcontrib><creatorcontrib>Wang, Jubo</creatorcontrib><creatorcontrib>Cai, Bing</creatorcontrib><creatorcontrib>Bai, Ximin</creatorcontrib><creatorcontrib>Zhu, Yiru</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Feng, Yi</au><au>Wang, Jubo</au><au>Cai, Bing</au><au>Bai, Ximin</au><au>Zhu, Yiru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2022-04</date><risdate>2022</risdate><volume>37</volume><issue>4</issue><spage>754</spage><epage>764</epage><pages>754-764</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract>Objective
This study aimed to investigate the regulatory effect of ivermectin (IVM) on energy metabolism in glioma progression, and provide a reference for the treatment of glioma.
Methods
Glioma cells were treated with IVM to measure cell viability, autophagy marker protein expression, ATP content, glucose uptake, pyruvate content, and expression of key enzymes of glycolysis. Glucose transporter 4 (GLUT4) or siGLUT4 was transfected in IVM treated U87 cells to investigate the effect of GLUT4 on cellular glycolysis and autophagy. The JAK2 inhibitor AZD‐1480 was introduced to explore the specific mechanism by which IVM regulates glycolysis and autophagy. Rat models of glioma xenograft were constructed and treated with 10 mg/kg IVM to observe tumor growth and examine the expression levels of GLUT4 and autophagy marker proteins in tumor tissues.
Results
IVM inhibited glioma cell survival and promoted cell death. IVM promoted LC3‐II protein expression and inhibited p62/SQSTM1 protein expression in glioma cells. IVM decreased adenosine‐triphosphate (ATP) and pyruvate content, promoted glucose uptake, and reduced HK2 and PFK1 protein expression in U87 cells. IVM inhibited GLUT4 protein expression, and overexpression of GLUT4 promoted glycolysis and inhibited autophagic cell death in U87 cells. IVM inhibited glycolysis by blocking GLUT4 mediated the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway activation. IVM inhibited tumor growth in vivo, decreased the protein expression of GLUT4, JAK2, HK2, and PFK1 in tumor tissues, decreased the phosphorylation levels of STAT3/STAT5, and promoted the expression of autophagy marker proteins.
Conclusions
IVM accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>34904774</pmid><doi>10.1002/tox.23440</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-5023-2422</orcidid></addata></record> |
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subjects | Adenosine Adenosine triphosphate Animal models Animals Apoptosis ATP Autophagic Cell Death - drug effects Autophagy Brain tumors Cell death Cell Line, Tumor Cell survival Cell viability Energy metabolism Glioma Glioma - metabolism Glioma cells Glucose Glucose transporter Glucose Transporter Type 4 - antagonists & inhibitors GLUT4 Glycolysis Humans Ivermectin Ivermectin - pharmacology Ivermectin - therapeutic use Janus kinase Janus kinase 2 Janus Kinases - metabolism Kinases Markers Metabolism Mortality Neoplasms Phosphorylation Protein expression Proteins Pyruvic acid Rats Signal Transduction Signaling STAT Transcription Factors - metabolism Stat3 protein Stat5 protein Survival the JAK/STAT signaling pathway Tissue Transcription Transducers Tumors Uptake Xenografts Xenotransplantation |
title | Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation |
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