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
Hauptverfasser: Feng, Yi, Wang, Jubo, Cai, Bing, Bai, Ximin, Zhu, Yiru
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container_issue 4
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container_title Environmental toxicology
container_volume 37
creator Feng, Yi
Wang, Jubo
Cai, Bing
Bai, Ximin
Zhu, Yiru
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
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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 &amp; 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 &amp; 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 &amp; 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 &amp; 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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 &amp; Fisheries Abstracts (ASFA) 3: Aquatic Pollution &amp; Environmental Quality</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Aquatic Science &amp; 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 &amp; 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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