Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development
A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no...
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| Veröffentlicht in: | Journal of cellular biochemistry 1997-10, Vol.67 (1), p.131-135 |
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| container_title | Journal of cellular biochemistry |
| container_volume | 67 |
| creator | Au, K.K. Liong, E. Li, J.Y. Li, P.S. Liew, C.C. Kwok, T.T. Choy, Y.M. Lee, C.Y. Fung, K.P. |
| description | A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no GLUT2, GLUT4, or GLUT5. The mRNA levels of GLUT1 and GLUT3 increased progressively in the tumour during development; however, there were no changes observable in mRNA levels of glucose transporters of all types in brain, liver, and heart of the host mice. These findings suggest that Ehrlich ascites tumor augments its glucose transport mechanism relative to other tissues in response to its unique growth needs. J. Cell. Biochem. 67:131–135, 1997. © 1997 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/(SICI)1097-4644(19971001)67:1<131::AID-JCB13>3.0.CO;2-K |
| format | Article |
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We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no GLUT2, GLUT4, or GLUT5. The mRNA levels of GLUT1 and GLUT3 increased progressively in the tumour during development; however, there were no changes observable in mRNA levels of glucose transporters of all types in brain, liver, and heart of the host mice. These findings suggest that Ehrlich ascites tumor augments its glucose transport mechanism relative to other tissues in response to its unique growth needs. J. Cell. Biochem. 67:131–135, 1997. © 1997 Wiley‐Liss, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/(SICI)1097-4644(19971001)67:1<131::AID-JCB13>3.0.CO;2-K</identifier><identifier>PMID: 9328846</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Blood Glucose - analysis ; Carcinoma, Ehrlich Tumor - genetics ; Carcinoma, Ehrlich Tumor - metabolism ; DNA, Complementary ; Ehrlich ascites tumor ; Food Deprivation ; Gene Expression Regulation, Neoplastic - physiology ; glucose transporter ; Glucose Transporter Type 1 ; Glucose Transporter Type 3 ; Humans ; Mice ; Monosaccharide Transport Proteins - genetics ; mRNA ; Nerve Tissue Proteins ; Organ Specificity ; RNA, Messenger - biosynthesis</subject><ispartof>Journal of cellular biochemistry, 1997-10, Vol.67 (1), p.131-135</ispartof><rights>Copyright © 1997 Wiley‐Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4053-17556faf62e28c45105e84ff22992dd2d8295f3951dacb24d23339b7ba8b226e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2F%28SICI%291097-4644%2819971001%2967%3A1%3C131%3A%3AAID-JCB13%3E3.0.CO%3B2-K$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2F%28SICI%291097-4644%2819971001%2967%3A1%3C131%3A%3AAID-JCB13%3E3.0.CO%3B2-K$$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/9328846$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Au, K.K.</creatorcontrib><creatorcontrib>Liong, E.</creatorcontrib><creatorcontrib>Li, J.Y.</creatorcontrib><creatorcontrib>Li, P.S.</creatorcontrib><creatorcontrib>Liew, C.C.</creatorcontrib><creatorcontrib>Kwok, T.T.</creatorcontrib><creatorcontrib>Choy, Y.M.</creatorcontrib><creatorcontrib>Lee, C.Y.</creatorcontrib><creatorcontrib>Fung, K.P.</creatorcontrib><title>Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no GLUT2, GLUT4, or GLUT5. The mRNA levels of GLUT1 and GLUT3 increased progressively in the tumour during development; however, there were no changes observable in mRNA levels of glucose transporters of all types in brain, liver, and heart of the host mice. These findings suggest that Ehrlich ascites tumor augments its glucose transport mechanism relative to other tissues in response to its unique growth needs. J. Cell. Biochem. 67:131–135, 1997. © 1997 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>Blood Glucose - analysis</subject><subject>Carcinoma, Ehrlich Tumor - genetics</subject><subject>Carcinoma, Ehrlich Tumor - metabolism</subject><subject>DNA, Complementary</subject><subject>Ehrlich ascites tumor</subject><subject>Food Deprivation</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>glucose transporter</subject><subject>Glucose Transporter Type 1</subject><subject>Glucose Transporter Type 3</subject><subject>Humans</subject><subject>Mice</subject><subject>Monosaccharide Transport Proteins - genetics</subject><subject>mRNA</subject><subject>Nerve Tissue Proteins</subject><subject>Organ Specificity</subject><subject>RNA, Messenger - biosynthesis</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtv1DAQhS0EKkvhJyD5CbUPWXxJ4nhBoG1atqGrrlRA7dvISZw2kFvtpGX_PQ5Z9gUkXmxpzsx3RnMQ-kjJnBLC3h59SeLkmBIpPD_0_SMqpXACPQ7Fgr6nnC4Wy-TU-xyfUP6Bz8k83rxj3sUTNNvPPEUzIjjxGKfsOXph7XdCiJScHaAD90aRH87QQ9JkRiurLS4bXF9dLnGlH3RlcVvg22rIWqtxb1Rju9b02ljcbzvXTLFqcszHobM7U5XZHVY2K3sn9UPdGpzpykHywZTN7a6Uj-C2q3XTv0TPClVZ_Wr3H6Jvn86-xufeerNK4uXay3wScI-KIAgLVYRMsyjzA0oCHflFwZiULM9ZHjEZFFwGNFdZyvyccc5lKlIVpYyFmh-iNxO3M-39oG0PdWnH1VSj28GCkJzSiIau8XpqzExrrdEFdKasldkCJTAmAjAmAuN1Ybwu_EkEQgEUXCIALhH4nQhwIBBvgMGFI7_erTCktc733F0ETr-Z9Mey0tu_bP_r-i_TqeDQ3oQuba9_7tHK_HDjXARwfbmC9enq5OZcMLjivwBtP7Yc</recordid><startdate>19971001</startdate><enddate>19971001</enddate><creator>Au, K.K.</creator><creator>Liong, E.</creator><creator>Li, J.Y.</creator><creator>Li, P.S.</creator><creator>Liew, C.C.</creator><creator>Kwok, T.T.</creator><creator>Choy, Y.M.</creator><creator>Lee, C.Y.</creator><creator>Fung, K.P.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>19971001</creationdate><title>Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development</title><author>Au, K.K. ; Liong, E. ; Li, J.Y. ; Li, P.S. ; Liew, C.C. ; Kwok, T.T. ; Choy, Y.M. ; Lee, C.Y. ; Fung, K.P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4053-17556faf62e28c45105e84ff22992dd2d8295f3951dacb24d23339b7ba8b226e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Blood Glucose - analysis</topic><topic>Carcinoma, Ehrlich Tumor - genetics</topic><topic>Carcinoma, Ehrlich Tumor - metabolism</topic><topic>DNA, Complementary</topic><topic>Ehrlich ascites tumor</topic><topic>Food Deprivation</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>glucose transporter</topic><topic>Glucose Transporter Type 1</topic><topic>Glucose Transporter Type 3</topic><topic>Humans</topic><topic>Mice</topic><topic>Monosaccharide Transport Proteins - genetics</topic><topic>mRNA</topic><topic>Nerve Tissue Proteins</topic><topic>Organ Specificity</topic><topic>RNA, Messenger - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Au, K.K.</creatorcontrib><creatorcontrib>Liong, E.</creatorcontrib><creatorcontrib>Li, J.Y.</creatorcontrib><creatorcontrib>Li, P.S.</creatorcontrib><creatorcontrib>Liew, C.C.</creatorcontrib><creatorcontrib>Kwok, T.T.</creatorcontrib><creatorcontrib>Choy, Y.M.</creatorcontrib><creatorcontrib>Lee, C.Y.</creatorcontrib><creatorcontrib>Fung, K.P.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Au, K.K.</au><au>Liong, E.</au><au>Li, J.Y.</au><au>Li, P.S.</au><au>Liew, C.C.</au><au>Kwok, T.T.</au><au>Choy, Y.M.</au><au>Lee, C.Y.</au><au>Fung, K.P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>1997-10-01</date><risdate>1997</risdate><volume>67</volume><issue>1</issue><spage>131</spage><epage>135</epage><pages>131-135</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>A common feature of many tumors is an increase in glucose catabolism during tumor growth. We studied the mechanism of this phenomenon by using Ehrlich ascites tumor bearing mice as the animal model. We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but no GLUT2, GLUT4, or GLUT5. The mRNA levels of GLUT1 and GLUT3 increased progressively in the tumour during development; however, there were no changes observable in mRNA levels of glucose transporters of all types in brain, liver, and heart of the host mice. These findings suggest that Ehrlich ascites tumor augments its glucose transport mechanism relative to other tissues in response to its unique growth needs. J. Cell. 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| subjects | Animals Blood Glucose - analysis Carcinoma, Ehrlich Tumor - genetics Carcinoma, Ehrlich Tumor - metabolism DNA, Complementary Ehrlich ascites tumor Food Deprivation Gene Expression Regulation, Neoplastic - physiology glucose transporter Glucose Transporter Type 1 Glucose Transporter Type 3 Humans Mice Monosaccharide Transport Proteins - genetics mRNA Nerve Tissue Proteins Organ Specificity RNA, Messenger - biosynthesis |
| title | Increases in mRNA levels of glucose transporters types 1 and 3 in Ehrlich ascites tumor cells during tumor development |
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