Dlx-2 is implicated in TGF-β- and Wnt-induced epithelial-mesenchymal, glycolytic switch, and mitochondrial repression by Snail activation
Epithelial-mesenchymal transition (EMT) and oncogenic metabolism (including glycolytic switch) are important for tumor development and progression. Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced...
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| Veröffentlicht in: | International journal of oncology 2015-04, Vol.46 (4), p.1768-1780 |
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| container_title | International journal of oncology |
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| creator | LEE, SU YEON JEON, HYUN MIN JU, MIN KYUNG JEONG, EUI KYONG KIM, CHO HEE YOO, MI-AE PARK, HYE GYEONG HAN, SONG IY KANG, HO SUNG |
| description | Epithelial-mesenchymal transition (EMT) and oncogenic metabolism (including glycolytic switch) are important for tumor development and progression. Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced by TGF-β and Wnt and regulates TGF-β- and Wnt-induced EMT and glycolytic switch by activating Snail. We also found that TGF-β/Wnt suppressed cytochrome c oxidase (COX), the terminal enzyme of the mitochondrial respiratory chain, in a Dlx-2/Snail-dependent manner. TGF-β/Wnt appeared to downregulate the expression of various COX subunits including COXVIc, COXVIIa and COXVIIc; among these COX subunits, COXVIc was a common target of TGF-β, Wnt, Dlx-2 and Snail, indicating that COXVIc downregulation plays an important role(s) in TGF-β/Wnt-induced COX inhibition. Taken together, our results showed that Dlx-2 is involved in TGF-β- and Wnt-induced EMT, glycolytic switch, and mitochondrial repression by Snail activation. |
| doi_str_mv | 10.3892/ijo.2015.2874 |
| format | Article |
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Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced by TGF-β and Wnt and regulates TGF-β- and Wnt-induced EMT and glycolytic switch by activating Snail. We also found that TGF-β/Wnt suppressed cytochrome c oxidase (COX), the terminal enzyme of the mitochondrial respiratory chain, in a Dlx-2/Snail-dependent manner. TGF-β/Wnt appeared to downregulate the expression of various COX subunits including COXVIc, COXVIIa and COXVIIc; among these COX subunits, COXVIc was a common target of TGF-β, Wnt, Dlx-2 and Snail, indicating that COXVIc downregulation plays an important role(s) in TGF-β/Wnt-induced COX inhibition. Taken together, our results showed that Dlx-2 is involved in TGF-β- and Wnt-induced EMT, glycolytic switch, and mitochondrial repression by Snail activation.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2015.2874</identifier><identifier>PMID: 25651912</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Animals ; Binding sites ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Cell Line, Tumor ; COXVIc ; Cytochrome ; Dlx-2 ; Dogs ; Epithelial-Mesenchymal Transition ; Female ; Glycolysis ; glycolytic switch ; HCT116 Cells ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Madin Darby Canine Kidney Cells ; MCF-7 Cells ; Metastasis ; Mitochondria - physiology ; Respiration ; Snail ; Snail Family Transcription Factors ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Transforming Growth Factor beta - metabolism ; Wnt Signaling Pathway</subject><ispartof>International journal of oncology, 2015-04, Vol.46 (4), p.1768-1780</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-542b948148ced4f115a9ea202e1ffa4ed63b77d86bbffadd89b3f346cfd8d54c3</citedby><cites>FETCH-LOGICAL-c392t-542b948148ced4f115a9ea202e1ffa4ed63b77d86bbffadd89b3f346cfd8d54c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25651912$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LEE, SU YEON</creatorcontrib><creatorcontrib>JEON, HYUN MIN</creatorcontrib><creatorcontrib>JU, MIN KYUNG</creatorcontrib><creatorcontrib>JEONG, EUI KYONG</creatorcontrib><creatorcontrib>KIM, CHO HEE</creatorcontrib><creatorcontrib>YOO, MI-AE</creatorcontrib><creatorcontrib>PARK, HYE GYEONG</creatorcontrib><creatorcontrib>HAN, SONG IY</creatorcontrib><creatorcontrib>KANG, HO SUNG</creatorcontrib><title>Dlx-2 is implicated in TGF-β- and Wnt-induced epithelial-mesenchymal, glycolytic switch, and mitochondrial repression by Snail activation</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Epithelial-mesenchymal transition (EMT) and oncogenic metabolism (including glycolytic switch) are important for tumor development and progression. Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced by TGF-β and Wnt and regulates TGF-β- and Wnt-induced EMT and glycolytic switch by activating Snail. We also found that TGF-β/Wnt suppressed cytochrome c oxidase (COX), the terminal enzyme of the mitochondrial respiratory chain, in a Dlx-2/Snail-dependent manner. TGF-β/Wnt appeared to downregulate the expression of various COX subunits including COXVIc, COXVIIa and COXVIIc; among these COX subunits, COXVIc was a common target of TGF-β, Wnt, Dlx-2 and Snail, indicating that COXVIc downregulation plays an important role(s) in TGF-β/Wnt-induced COX inhibition. Taken together, our results showed that Dlx-2 is involved in TGF-β- and Wnt-induced EMT, glycolytic switch, and mitochondrial repression by Snail activation.</description><subject>Animals</subject><subject>Binding sites</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>COXVIc</subject><subject>Cytochrome</subject><subject>Dlx-2</subject><subject>Dogs</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Glycolysis</subject><subject>glycolytic switch</subject><subject>HCT116 Cells</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Madin Darby Canine Kidney Cells</subject><subject>MCF-7 Cells</subject><subject>Metastasis</subject><subject>Mitochondria - physiology</subject><subject>Respiration</subject><subject>Snail</subject><subject>Snail Family Transcription Factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Wnt Signaling Pathway</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNo9kM1uFSEUx0mjsbW67NaQuHBTrnzODMum9sOkiQtrXE4YYLzcMDAFrnZeoY_TB_GZ5PbWrjhwfud_yA-AE4JXrJP0s9vEFcVErGjX8gNwRFpJEOWUvao1JhI1nMlD8DbnDcZUCEzegEMqGkEkoUfg4Yu_RxS6DN00e6dVsQa6AG-vLtHfRwRVMPBnKMgFs9W1ZWdX1tY75dFksw16vUzKn8JfftHRL8VpmP-4otenT6OTK1GvYzCpTsBk52RzdjHAYYHfg3IeKl3cb1Xq2zvwelQ-2_fP5zH4cXlxe36Nbr5dfT0_u0GaSVqQ4HSQvCO8q__hIyFCSasoppaMo-LWNGxoW9M1w1DvxnRyYCPjjR5NZwTX7Bh83OfOKd5tbS79Jm5TqCt7IhllDHMpKoX2lE4x52THfk5uUmnpCe535vtqvt-Z73fmK__hOXU7TNa80P9VV-DTHshzNeNMzC9MTUK8QZgj0jYd-we1l48F</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>LEE, SU YEON</creator><creator>JEON, HYUN MIN</creator><creator>JU, MIN KYUNG</creator><creator>JEONG, EUI KYONG</creator><creator>KIM, CHO HEE</creator><creator>YOO, MI-AE</creator><creator>PARK, HYE GYEONG</creator><creator>HAN, SONG IY</creator><creator>KANG, HO SUNG</creator><general>D.A. 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KANG, HO SUNG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-542b948148ced4f115a9ea202e1ffa4ed63b77d86bbffadd89b3f346cfd8d54c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Binding sites</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>COXVIc</topic><topic>Cytochrome</topic><topic>Dlx-2</topic><topic>Dogs</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Glycolysis</topic><topic>glycolytic switch</topic><topic>HCT116 Cells</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Madin Darby Canine Kidney Cells</topic><topic>MCF-7 Cells</topic><topic>Metastasis</topic><topic>Mitochondria - physiology</topic><topic>Respiration</topic><topic>Snail</topic><topic>Snail Family Transcription Factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LEE, SU YEON</creatorcontrib><creatorcontrib>JEON, HYUN MIN</creatorcontrib><creatorcontrib>JU, MIN KYUNG</creatorcontrib><creatorcontrib>JEONG, EUI KYONG</creatorcontrib><creatorcontrib>KIM, CHO HEE</creatorcontrib><creatorcontrib>YOO, MI-AE</creatorcontrib><creatorcontrib>PARK, HYE GYEONG</creatorcontrib><creatorcontrib>HAN, SONG IY</creatorcontrib><creatorcontrib>KANG, HO SUNG</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LEE, SU YEON</au><au>JEON, HYUN MIN</au><au>JU, MIN KYUNG</au><au>JEONG, EUI KYONG</au><au>KIM, CHO HEE</au><au>YOO, MI-AE</au><au>PARK, HYE GYEONG</au><au>HAN, SONG IY</au><au>KANG, HO SUNG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dlx-2 is implicated in TGF-β- and Wnt-induced epithelial-mesenchymal, glycolytic switch, and mitochondrial repression by Snail activation</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>46</volume><issue>4</issue><spage>1768</spage><epage>1780</epage><pages>1768-1780</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>Epithelial-mesenchymal transition (EMT) and oncogenic metabolism (including glycolytic switch) are important for tumor development and progression. Here, we show that Dlx-2, one of distal-less (Dlx) homeobox genes, induces EMT and glycolytic switch by activation of Snail. In addition, it was induced by TGF-β and Wnt and regulates TGF-β- and Wnt-induced EMT and glycolytic switch by activating Snail. We also found that TGF-β/Wnt suppressed cytochrome c oxidase (COX), the terminal enzyme of the mitochondrial respiratory chain, in a Dlx-2/Snail-dependent manner. TGF-β/Wnt appeared to downregulate the expression of various COX subunits including COXVIc, COXVIIa and COXVIIc; among these COX subunits, COXVIc was a common target of TGF-β, Wnt, Dlx-2 and Snail, indicating that COXVIc downregulation plays an important role(s) in TGF-β/Wnt-induced COX inhibition. Taken together, our results showed that Dlx-2 is involved in TGF-β- and Wnt-induced EMT, glycolytic switch, and mitochondrial repression by Snail activation.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>25651912</pmid><doi>10.3892/ijo.2015.2874</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Binding sites Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Cell Line, Tumor COXVIc Cytochrome Dlx-2 Dogs Epithelial-Mesenchymal Transition Female Glycolysis glycolytic switch HCT116 Cells Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Madin Darby Canine Kidney Cells MCF-7 Cells Metastasis Mitochondria - physiology Respiration Snail Snail Family Transcription Factors Transcription Factors - genetics Transcription Factors - metabolism Transforming Growth Factor beta - metabolism Wnt Signaling Pathway |
| title | Dlx-2 is implicated in TGF-β- and Wnt-induced epithelial-mesenchymal, glycolytic switch, and mitochondrial repression by Snail activation |
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