Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo
Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments and . The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes,...
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| Veröffentlicht in: | Journal of gastrointestinal oncology 2020-12, Vol.11 (6), p.1164-1185 |
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| container_title | Journal of gastrointestinal oncology |
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| creator | Cui, Ge Huang, Yuxuan Feng, Wenming Yao, Yunliang Zhou, Hongchang Li, Xining Gong, Hui Liu, Jun Luo, Yifan Sun, Yandi Zhang, Mengya Luo, Yan Zhang, Ting |
| description | Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments
and
.
The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in
-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with
-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected.
The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced
(P |
| doi_str_mv | 10.21037/jgo-20-474 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7807285</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2478772600</sourcerecordid><originalsourceid>FETCH-LOGICAL-c381t-6a0ad288eb7295ff01df1a79afaa2441173297223fe6517c137d6b0cf2cf16cd3</originalsourceid><addsrcrecordid>eNpVkc1qGzEURkVpqEOSVfdFy0JRq5-Z0WhTKKZJCoZsEshOXGskW2ZGciXZkNfoE0d2EpNqI4l7dO4VH0KfGf3OGRXyx2YVCaekkc0HdM45U6ST6vFjPVPZk65XbIauct7QuhrV0pZ_QjMhmrZTip2jf_M4xoANBGMTgZyj8VDsgEuCkE3y20IYtmF9ADJejTsTs8WTLbCMo88ThjBg806CjR1HDKb4vS9P2AcMeO1Xa_L21oa9TzFMNpRDtVIpHi3Hyz5eojMHY7ZXr_sFerj-fT-_JYu7mz_zXwtiRM8K6YDCwPveLiVXrXOUDY6BVOAAeNMwJgVXknPhbNcyaZiQQ7ekxnHjWGcGcYF-vni3u-VkB1PnSTDqbfITpCcdwev_K8Gv9Sruteyp5H1bBV9fBSn-3dlc9OTz4fcQbNxlzRvZS8k7Siv67QU1KeacrDu1YVQfg9Q1SM2prkFW-sv7yU7sW2ziGc6MnXA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2478772600</pqid></control><display><type>article</type><title>Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo</title><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Cui, Ge ; Huang, Yuxuan ; Feng, Wenming ; Yao, Yunliang ; Zhou, Hongchang ; Li, Xining ; Gong, Hui ; Liu, Jun ; Luo, Yifan ; Sun, Yandi ; Zhang, Mengya ; Luo, Yan ; Zhang, Ting</creator><creatorcontrib>Cui, Ge ; Huang, Yuxuan ; Feng, Wenming ; Yao, Yunliang ; Zhou, Hongchang ; Li, Xining ; Gong, Hui ; Liu, Jun ; Luo, Yifan ; Sun, Yandi ; Zhang, Mengya ; Luo, Yan ; Zhang, Ting</creatorcontrib><description>Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments
and
.
The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in
-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with
-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected.
The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced
(P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05).
can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression.</description><identifier>ISSN: 2078-6891</identifier><identifier>EISSN: 2219-679X</identifier><identifier>DOI: 10.21037/jgo-20-474</identifier><identifier>PMID: 33456991</identifier><language>eng</language><publisher>China: AME Publishing Company</publisher><subject>Original</subject><ispartof>Journal of gastrointestinal oncology, 2020-12, Vol.11 (6), p.1164-1185</ispartof><rights>2020 Journal of Gastrointestinal Oncology. All rights reserved.</rights><rights>2020 Journal of Gastrointestinal Oncology. All rights reserved. 2020 Journal of Gastrointestinal Oncology.</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-6a0ad288eb7295ff01df1a79afaa2441173297223fe6517c137d6b0cf2cf16cd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7807285/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7807285/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33456991$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cui, Ge</creatorcontrib><creatorcontrib>Huang, Yuxuan</creatorcontrib><creatorcontrib>Feng, Wenming</creatorcontrib><creatorcontrib>Yao, Yunliang</creatorcontrib><creatorcontrib>Zhou, Hongchang</creatorcontrib><creatorcontrib>Li, Xining</creatorcontrib><creatorcontrib>Gong, Hui</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><creatorcontrib>Luo, Yifan</creatorcontrib><creatorcontrib>Sun, Yandi</creatorcontrib><creatorcontrib>Zhang, Mengya</creatorcontrib><creatorcontrib>Luo, Yan</creatorcontrib><creatorcontrib>Zhang, Ting</creatorcontrib><title>Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo</title><title>Journal of gastrointestinal oncology</title><addtitle>J Gastrointest Oncol</addtitle><description>Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments
and
.
The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in
-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with
-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected.
The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced
(P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05).
can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression.</description><subject>Original</subject><issn>2078-6891</issn><issn>2219-679X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNpVkc1qGzEURkVpqEOSVfdFy0JRq5-Z0WhTKKZJCoZsEshOXGskW2ZGciXZkNfoE0d2EpNqI4l7dO4VH0KfGf3OGRXyx2YVCaekkc0HdM45U6ST6vFjPVPZk65XbIauct7QuhrV0pZ_QjMhmrZTip2jf_M4xoANBGMTgZyj8VDsgEuCkE3y20IYtmF9ADJejTsTs8WTLbCMo88ThjBg806CjR1HDKb4vS9P2AcMeO1Xa_L21oa9TzFMNpRDtVIpHi3Hyz5eojMHY7ZXr_sFerj-fT-_JYu7mz_zXwtiRM8K6YDCwPveLiVXrXOUDY6BVOAAeNMwJgVXknPhbNcyaZiQQ7ekxnHjWGcGcYF-vni3u-VkB1PnSTDqbfITpCcdwev_K8Gv9Sruteyp5H1bBV9fBSn-3dlc9OTz4fcQbNxlzRvZS8k7Siv67QU1KeacrDu1YVQfg9Q1SM2prkFW-sv7yU7sW2ziGc6MnXA</recordid><startdate>202012</startdate><enddate>202012</enddate><creator>Cui, Ge</creator><creator>Huang, Yuxuan</creator><creator>Feng, Wenming</creator><creator>Yao, Yunliang</creator><creator>Zhou, Hongchang</creator><creator>Li, Xining</creator><creator>Gong, Hui</creator><creator>Liu, Jun</creator><creator>Luo, Yifan</creator><creator>Sun, Yandi</creator><creator>Zhang, Mengya</creator><creator>Luo, Yan</creator><creator>Zhang, Ting</creator><general>AME Publishing Company</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202012</creationdate><title>Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo</title><author>Cui, Ge ; Huang, Yuxuan ; Feng, Wenming ; Yao, Yunliang ; Zhou, Hongchang ; Li, Xining ; Gong, Hui ; Liu, Jun ; Luo, Yifan ; Sun, Yandi ; Zhang, Mengya ; Luo, Yan ; Zhang, Ting</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-6a0ad288eb7295ff01df1a79afaa2441173297223fe6517c137d6b0cf2cf16cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Original</topic><toplevel>online_resources</toplevel><creatorcontrib>Cui, Ge</creatorcontrib><creatorcontrib>Huang, Yuxuan</creatorcontrib><creatorcontrib>Feng, Wenming</creatorcontrib><creatorcontrib>Yao, Yunliang</creatorcontrib><creatorcontrib>Zhou, Hongchang</creatorcontrib><creatorcontrib>Li, Xining</creatorcontrib><creatorcontrib>Gong, Hui</creatorcontrib><creatorcontrib>Liu, Jun</creatorcontrib><creatorcontrib>Luo, Yifan</creatorcontrib><creatorcontrib>Sun, Yandi</creatorcontrib><creatorcontrib>Zhang, Mengya</creatorcontrib><creatorcontrib>Luo, Yan</creatorcontrib><creatorcontrib>Zhang, Ting</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of gastrointestinal oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cui, Ge</au><au>Huang, Yuxuan</au><au>Feng, Wenming</au><au>Yao, Yunliang</au><au>Zhou, Hongchang</au><au>Li, Xining</au><au>Gong, Hui</au><au>Liu, Jun</au><au>Luo, Yifan</au><au>Sun, Yandi</au><au>Zhang, Mengya</au><au>Luo, Yan</au><au>Zhang, Ting</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo</atitle><jtitle>Journal of gastrointestinal oncology</jtitle><addtitle>J Gastrointest Oncol</addtitle><date>2020-12</date><risdate>2020</risdate><volume>11</volume><issue>6</issue><spage>1164</spage><epage>1185</epage><pages>1164-1185</pages><issn>2078-6891</issn><eissn>2219-679X</eissn><abstract>Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments
and
.
The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in
-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with
-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected.
The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced
(P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05).
can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression.</abstract><cop>China</cop><pub>AME Publishing Company</pub><pmid>33456991</pmid><doi>10.21037/jgo-20-474</doi><tpages>22</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 2078-6891 2219-679X |
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| source | EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Original |
| title | Colon cancer-associated transcript-1 enhances glucose metabolism and colon cancer cell activity in a high-glucose environment in vitro and in vivo |
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