The mitochondrial retrograde signaling regulates Wnt signaling to promote tumorigenesis in colon cancer
Cancer cells are known to upregulate aerobic glycolysis to promote growth, proliferation, and survival. However, the role of mitochondrial respiration in tumorigenesis remains elusive. Here we report that inhibition of mitochondrial function by silencing TFAM, a key transcription factor essential fo...
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| Veröffentlicht in: | Cell death and differentiation 2019-10, Vol.26 (10), p.1955-1969 |
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| container_title | Cell death and differentiation |
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| creator | Wen, Yang-An Xiong, Xiaopeng Scott, Timothy Li, Austin T. Wang, Chi Weiss, Heidi L. Tan, Li Bradford, Emily Fan, Teresa W. M. Chandel, Navdeep S. Barrett, Terrence A. Gao, Tianyan |
| description | Cancer cells are known to upregulate aerobic glycolysis to promote growth, proliferation, and survival. However, the role of mitochondrial respiration in tumorigenesis remains elusive. Here we report that inhibition of mitochondrial function by silencing TFAM, a key transcription factor essential for mitochondrial DNA (mtDNA) replication and the transcription of mtDNA-encoded genes, markedly reduced tumor-initiating potential of colon cancer cells. Knockdown of TFAM significantly decreased mitochondrial respiration in colon cancer cells; however, the cellular levels of ATP remained largely unchanged as a result of increased glycolysis. This metabolic alteration rendered cancer cells highly susceptible to glucose deprivation. Interestingly, upregulation of glycolysis was independent of hypoxia-inducible factor-1 (HIF1) as TFAM knockdown cells fail to stabilize HIF1α under hypoxic conditions. Moreover, knockdown of TFAM results in decreased expression of genes-associated cancer stem cells downstream of Wnt/β-catenin signaling. Metabolic analysis reveals that the level of α-ketoglutarate (α-KG) was significantly upregulated in TFAM knockout cells. Silencing of prolyl hydroxylase domain-containing protein 2 (PHD2), a α-KG-dependent dioxyenase, rescued the expression of target genes of both HIF1α and Wnt/β-catenin. Furthermore, intestinal-specific knockout of TFAM prevents tumor formation in Apc-mutant mouse models of colon cancer. Taken together, our findings identify a novel role of mitochondria-mediated retrograde signaling in regulating Wnt signaling and tumor initiation in colon cancer. |
| doi_str_mv | 10.1038/s41418-018-0265-6 |
| format | Article |
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This metabolic alteration rendered cancer cells highly susceptible to glucose deprivation. Interestingly, upregulation of glycolysis was independent of hypoxia-inducible factor-1 (HIF1) as TFAM knockdown cells fail to stabilize HIF1α under hypoxic conditions. Moreover, knockdown of TFAM results in decreased expression of genes-associated cancer stem cells downstream of Wnt/β-catenin signaling. Metabolic analysis reveals that the level of α-ketoglutarate (α-KG) was significantly upregulated in TFAM knockout cells. Silencing of prolyl hydroxylase domain-containing protein 2 (PHD2), a α-KG-dependent dioxyenase, rescued the expression of target genes of both HIF1α and Wnt/β-catenin. Furthermore, intestinal-specific knockout of TFAM prevents tumor formation in Apc-mutant mouse models of colon cancer. Taken together, our findings identify a novel role of mitochondria-mediated retrograde signaling in regulating Wnt signaling and tumor initiation in colon cancer.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/s41418-018-0265-6</identifier><identifier>PMID: 30659235</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/106 ; 13/89 ; 13/95 ; 38/39 ; 631/67/2327 ; 64/60 ; 692/308/1426 ; 82/80 ; Adenomatous polyposis coli ; Animal models ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Cycle Analysis ; Cell proliferation ; Colon cancer ; Colorectal cancer ; DNA biosynthesis ; Electron transport ; Gene silencing ; Glycolysis ; Hypoxia-inducible factor 1 ; Hypoxia-inducible factor 1a ; Intestine ; Ketoglutaric acid ; Life Sciences ; Metabolism ; Mitochondrial DNA ; Prolyl hydroxylase ; Respiration ; Retrograde transport ; Stem cell transplantation ; Stem Cells ; Tumorigenesis ; Wnt protein ; β-Catenin</subject><ispartof>Cell death and differentiation, 2019-10, Vol.26 (10), p.1955-1969</ispartof><rights>ADMC Associazione Differenziamento e Morte Cellulare 2019</rights><rights>2019© ADMC Associazione Differenziamento e Morte Cellulare 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-cae2ccb55ecb7a0bf78ae69425958b553a6bbc11b62522a145c9a983096d98e43</citedby><cites>FETCH-LOGICAL-c536t-cae2ccb55ecb7a0bf78ae69425958b553a6bbc11b62522a145c9a983096d98e43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748256/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748256/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30659235$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wen, Yang-An</creatorcontrib><creatorcontrib>Xiong, Xiaopeng</creatorcontrib><creatorcontrib>Scott, Timothy</creatorcontrib><creatorcontrib>Li, Austin T.</creatorcontrib><creatorcontrib>Wang, Chi</creatorcontrib><creatorcontrib>Weiss, Heidi L.</creatorcontrib><creatorcontrib>Tan, Li</creatorcontrib><creatorcontrib>Bradford, Emily</creatorcontrib><creatorcontrib>Fan, Teresa W. M.</creatorcontrib><creatorcontrib>Chandel, Navdeep S.</creatorcontrib><creatorcontrib>Barrett, Terrence A.</creatorcontrib><creatorcontrib>Gao, Tianyan</creatorcontrib><title>The mitochondrial retrograde signaling regulates Wnt signaling to promote tumorigenesis in colon cancer</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Cancer cells are known to upregulate aerobic glycolysis to promote growth, proliferation, and survival. However, the role of mitochondrial respiration in tumorigenesis remains elusive. Here we report that inhibition of mitochondrial function by silencing TFAM, a key transcription factor essential for mitochondrial DNA (mtDNA) replication and the transcription of mtDNA-encoded genes, markedly reduced tumor-initiating potential of colon cancer cells. Knockdown of TFAM significantly decreased mitochondrial respiration in colon cancer cells; however, the cellular levels of ATP remained largely unchanged as a result of increased glycolysis. This metabolic alteration rendered cancer cells highly susceptible to glucose deprivation. Interestingly, upregulation of glycolysis was independent of hypoxia-inducible factor-1 (HIF1) as TFAM knockdown cells fail to stabilize HIF1α under hypoxic conditions. Moreover, knockdown of TFAM results in decreased expression of genes-associated cancer stem cells downstream of Wnt/β-catenin signaling. Metabolic analysis reveals that the level of α-ketoglutarate (α-KG) was significantly upregulated in TFAM knockout cells. Silencing of prolyl hydroxylase domain-containing protein 2 (PHD2), a α-KG-dependent dioxyenase, rescued the expression of target genes of both HIF1α and Wnt/β-catenin. Furthermore, intestinal-specific knockout of TFAM prevents tumor formation in Apc-mutant mouse models of colon cancer. Taken together, our findings identify a novel role of mitochondria-mediated retrograde signaling in regulating Wnt signaling and tumor initiation in colon cancer.</description><subject>13/106</subject><subject>13/89</subject><subject>13/95</subject><subject>38/39</subject><subject>631/67/2327</subject><subject>64/60</subject><subject>692/308/1426</subject><subject>82/80</subject><subject>Adenomatous polyposis coli</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Cycle Analysis</subject><subject>Cell proliferation</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>DNA biosynthesis</subject><subject>Electron transport</subject><subject>Gene silencing</subject><subject>Glycolysis</subject><subject>Hypoxia-inducible factor 1</subject><subject>Hypoxia-inducible factor 1a</subject><subject>Intestine</subject><subject>Ketoglutaric acid</subject><subject>Life Sciences</subject><subject>Metabolism</subject><subject>Mitochondrial DNA</subject><subject>Prolyl hydroxylase</subject><subject>Respiration</subject><subject>Retrograde transport</subject><subject>Stem cell transplantation</subject><subject>Stem Cells</subject><subject>Tumorigenesis</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>1350-9047</issn><issn>1476-5403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kUtLxDAUhYMovn-AGym4rubdZiOI-ALBjeIypJk7nUibjEkq-O_NMD4XLm4Szj35bsJB6IjgU4JZe5Y44aSt8aqoFLXcQLuEN7IWHLPNcmYC1wrzZgftpfSCMZaNkttoh2EpFGViF_WPC6hGl4NdBD-LzgxVhBxDH80MquR6bwbn-yL202AypOrZ5196DtUyhjFkqPI0huh68JBcqpyvbBhCWY23EA_Q1twMCQ4_9330dH31eHlb3z_c3F1e3NdWMJlra4Ba2wkBtmsM7uZNa0AqToUSbZGZkV1nCekkFZQawoVVRrUMKzlTLXC2j87X3OXUjTCz4HM0g15GN5r4roNx-m_Hu4Xuw5uWDW-pkAVw8gmI4XWClPVLmGL5bdKUtgI3EnNaXGTtsjGkFGH-PYFgvcpGr7PReFUlG70iH_9-2veNrzCKga4NqbR8D_Fn9P_UDynZnR0</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Wen, Yang-An</creator><creator>Xiong, Xiaopeng</creator><creator>Scott, Timothy</creator><creator>Li, Austin T.</creator><creator>Wang, Chi</creator><creator>Weiss, Heidi L.</creator><creator>Tan, Li</creator><creator>Bradford, Emily</creator><creator>Fan, Teresa W. 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M.</au><au>Chandel, Navdeep S.</au><au>Barrett, Terrence A.</au><au>Gao, Tianyan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The mitochondrial retrograde signaling regulates Wnt signaling to promote tumorigenesis in colon cancer</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2019-10-01</date><risdate>2019</risdate><volume>26</volume><issue>10</issue><spage>1955</spage><epage>1969</epage><pages>1955-1969</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Cancer cells are known to upregulate aerobic glycolysis to promote growth, proliferation, and survival. However, the role of mitochondrial respiration in tumorigenesis remains elusive. Here we report that inhibition of mitochondrial function by silencing TFAM, a key transcription factor essential for mitochondrial DNA (mtDNA) replication and the transcription of mtDNA-encoded genes, markedly reduced tumor-initiating potential of colon cancer cells. Knockdown of TFAM significantly decreased mitochondrial respiration in colon cancer cells; however, the cellular levels of ATP remained largely unchanged as a result of increased glycolysis. This metabolic alteration rendered cancer cells highly susceptible to glucose deprivation. Interestingly, upregulation of glycolysis was independent of hypoxia-inducible factor-1 (HIF1) as TFAM knockdown cells fail to stabilize HIF1α under hypoxic conditions. Moreover, knockdown of TFAM results in decreased expression of genes-associated cancer stem cells downstream of Wnt/β-catenin signaling. Metabolic analysis reveals that the level of α-ketoglutarate (α-KG) was significantly upregulated in TFAM knockout cells. Silencing of prolyl hydroxylase domain-containing protein 2 (PHD2), a α-KG-dependent dioxyenase, rescued the expression of target genes of both HIF1α and Wnt/β-catenin. Furthermore, intestinal-specific knockout of TFAM prevents tumor formation in Apc-mutant mouse models of colon cancer. Taken together, our findings identify a novel role of mitochondria-mediated retrograde signaling in regulating Wnt signaling and tumor initiation in colon cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30659235</pmid><doi>10.1038/s41418-018-0265-6</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/106 13/89 13/95 38/39 631/67/2327 64/60 692/308/1426 82/80 Adenomatous polyposis coli Animal models Apoptosis Biochemistry Biomedical and Life Sciences Cell Biology Cell Cycle Analysis Cell proliferation Colon cancer Colorectal cancer DNA biosynthesis Electron transport Gene silencing Glycolysis Hypoxia-inducible factor 1 Hypoxia-inducible factor 1a Intestine Ketoglutaric acid Life Sciences Metabolism Mitochondrial DNA Prolyl hydroxylase Respiration Retrograde transport Stem cell transplantation Stem Cells Tumorigenesis Wnt protein β-Catenin |
| title | The mitochondrial retrograde signaling regulates Wnt signaling to promote tumorigenesis in colon cancer |
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