Genome-Wide Study of Hypomethylated and Induced Genes in Patients with Liver Cancer Unravels Novel Anticancer Targets
We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for thei...
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| Veröffentlicht in: | Clinical cancer research 2014-06, Vol.20 (12), p.3118-3132 |
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| creator | STEFANSKA, Barbara CHEISHVILI, David RAQIB, Rubhana TANVIR, Imrana HASEEB AHMED KHAN RABBANI, Shafaat A SZYF, Moshe SUDERMAN, Matthew ARAKELIAN, Ani JIAN HUANG HALLETT, Michael HAN, Ze-Guang AL-MAHTAB, Mamun SHEIKH MOHAMMAD FAZLE AKBAR WASIF ALI KHAN |
| description | We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.
We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.
Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR. |
| doi_str_mv | 10.1158/1078-0432.CCR-13-0283 |
| format | Article |
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We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.
Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-13-0283</identifier><identifier>PMID: 24763612</identifier><identifier>CODEN: CCREF4</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Biological and medical sciences ; Biomarkers, Tumor - genetics ; Carcinoma, Hepatocellular - genetics ; Carrier Proteins - antagonists & inhibitors ; Carrier Proteins - genetics ; Cell Movement ; Cell Proliferation ; Cysteine Endopeptidases - chemistry ; Cysteine Endopeptidases - genetics ; DNA Methylation ; Exosome Multienzyme Ribonuclease Complex - antagonists & inhibitors ; Exosome Multienzyme Ribonuclease Complex - genetics ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression Regulation, Neoplastic ; Genome-Wide Association Study ; Humans ; Intercellular Signaling Peptides and Proteins - genetics ; Liver Neoplasms - genetics ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Methyltransferases - antagonists & inhibitors ; Methyltransferases - genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Nerve Tissue Proteins - genetics ; Pharmacology. Drug treatments ; Promoter Regions, Genetic - genetics ; RNA, Small Interfering - genetics ; RNA-Binding Proteins - antagonists & inhibitors ; RNA-Binding Proteins - genetics ; Signal Transduction ; Tumors</subject><ispartof>Clinical cancer research, 2014-06, Vol.20 (12), p.3118-3132</ispartof><rights>2015 INIST-CNRS</rights><rights>2014 American Association for Cancer Research.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-758d14e54253fca1293b86c2659e8ac7bcad657c6ee251c4da0355018ac323a63</citedby><cites>FETCH-LOGICAL-c490t-758d14e54253fca1293b86c2659e8ac7bcad657c6ee251c4da0355018ac323a63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28538895$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24763612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STEFANSKA, Barbara</creatorcontrib><creatorcontrib>CHEISHVILI, David</creatorcontrib><creatorcontrib>RAQIB, Rubhana</creatorcontrib><creatorcontrib>TANVIR, Imrana</creatorcontrib><creatorcontrib>HASEEB AHMED KHAN</creatorcontrib><creatorcontrib>RABBANI, Shafaat A</creatorcontrib><creatorcontrib>SZYF, Moshe</creatorcontrib><creatorcontrib>SUDERMAN, Matthew</creatorcontrib><creatorcontrib>ARAKELIAN, Ani</creatorcontrib><creatorcontrib>JIAN HUANG</creatorcontrib><creatorcontrib>HALLETT, Michael</creatorcontrib><creatorcontrib>HAN, Ze-Guang</creatorcontrib><creatorcontrib>AL-MAHTAB, Mamun</creatorcontrib><creatorcontrib>SHEIKH MOHAMMAD FAZLE AKBAR</creatorcontrib><creatorcontrib>WASIF ALI KHAN</creatorcontrib><title>Genome-Wide Study of Hypomethylated and Induced Genes in Patients with Liver Cancer Unravels Novel Anticancer Targets</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.
We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.
Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carrier Proteins - antagonists & inhibitors</subject><subject>Carrier Proteins - genetics</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cysteine Endopeptidases - chemistry</subject><subject>Cysteine Endopeptidases - genetics</subject><subject>DNA Methylation</subject><subject>Exosome Multienzyme Ribonuclease Complex - antagonists & inhibitors</subject><subject>Exosome Multienzyme Ribonuclease Complex - genetics</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methyltransferases - antagonists & inhibitors</subject><subject>Methyltransferases - genetics</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Pharmacology. Drug treatments</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA-Binding Proteins - antagonists & inhibitors</subject><subject>RNA-Binding Proteins - genetics</subject><subject>Signal Transduction</subject><subject>Tumors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1vEzEQhi1ERT_gJ4B8QeKyxWOvvc6xWpW2UlSqfoij5diz1GjjDba3KP8eR0nh9I5mnhnLDyEfgZ0DSP0VWKcb1gp-3vf3DYiGcS3ekBOQsmsEV_JtrV-ZY3Ka8y_GoAXWviPHvO2UUMBPyHyFcVpj8yN4pA9l9ls6DfR6u6nN8rwdbUFPbfT0JvrZ1brymGmI9M6WgLFk-ieUZ7oML5hob6Or8RSTfcEx09upBr2IJbj95NGmn1jye3I02DHjh0Oekadvl4_9dbP8fnXTXywb1y5YaTqpPbQoWy7F4CzwhVhp5ernFqit61bOeiU7pxC5BNd6y4SUDOpMcGGVOCNf9nc3afo9Yy5mHbLDcbQRpzkbkEIqDlpBReUedWnKOeFgNimsbdoaYGZn3Oxsmp1NU40bEGZnvO59Ojwxr9bo_229Kq7A5wNgs7PjkKqJkP9zWgqtF1L8Bab8iXw</recordid><startdate>20140615</startdate><enddate>20140615</enddate><creator>STEFANSKA, Barbara</creator><creator>CHEISHVILI, David</creator><creator>RAQIB, Rubhana</creator><creator>TANVIR, Imrana</creator><creator>HASEEB AHMED KHAN</creator><creator>RABBANI, Shafaat A</creator><creator>SZYF, Moshe</creator><creator>SUDERMAN, Matthew</creator><creator>ARAKELIAN, Ani</creator><creator>JIAN HUANG</creator><creator>HALLETT, Michael</creator><creator>HAN, Ze-Guang</creator><creator>AL-MAHTAB, Mamun</creator><creator>SHEIKH MOHAMMAD FAZLE AKBAR</creator><creator>WASIF ALI KHAN</creator><general>American Association for Cancer Research</general><scope>IQODW</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>20140615</creationdate><title>Genome-Wide Study of Hypomethylated and Induced Genes in Patients with Liver Cancer Unravels Novel Anticancer Targets</title><author>STEFANSKA, Barbara ; CHEISHVILI, David ; RAQIB, Rubhana ; TANVIR, Imrana ; HASEEB AHMED KHAN ; RABBANI, Shafaat A ; SZYF, Moshe ; SUDERMAN, Matthew ; ARAKELIAN, Ani ; JIAN HUANG ; HALLETT, Michael ; HAN, Ze-Guang ; AL-MAHTAB, Mamun ; SHEIKH MOHAMMAD FAZLE AKBAR ; WASIF ALI KHAN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-758d14e54253fca1293b86c2659e8ac7bcad657c6ee251c4da0355018ac323a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carrier Proteins - antagonists & inhibitors</topic><topic>Carrier Proteins - genetics</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cysteine Endopeptidases - chemistry</topic><topic>Cysteine Endopeptidases - genetics</topic><topic>DNA Methylation</topic><topic>Exosome Multienzyme Ribonuclease Complex - antagonists & inhibitors</topic><topic>Exosome Multienzyme Ribonuclease Complex - genetics</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methyltransferases - antagonists & inhibitors</topic><topic>Methyltransferases - genetics</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Pharmacology. Drug treatments</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA-Binding Proteins - antagonists & inhibitors</topic><topic>RNA-Binding Proteins - genetics</topic><topic>Signal Transduction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STEFANSKA, Barbara</creatorcontrib><creatorcontrib>CHEISHVILI, David</creatorcontrib><creatorcontrib>RAQIB, Rubhana</creatorcontrib><creatorcontrib>TANVIR, Imrana</creatorcontrib><creatorcontrib>HASEEB AHMED KHAN</creatorcontrib><creatorcontrib>RABBANI, Shafaat A</creatorcontrib><creatorcontrib>SZYF, Moshe</creatorcontrib><creatorcontrib>SUDERMAN, Matthew</creatorcontrib><creatorcontrib>ARAKELIAN, Ani</creatorcontrib><creatorcontrib>JIAN HUANG</creatorcontrib><creatorcontrib>HALLETT, Michael</creatorcontrib><creatorcontrib>HAN, Ze-Guang</creatorcontrib><creatorcontrib>AL-MAHTAB, Mamun</creatorcontrib><creatorcontrib>SHEIKH MOHAMMAD FAZLE AKBAR</creatorcontrib><creatorcontrib>WASIF ALI KHAN</creatorcontrib><collection>Pascal-Francis</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>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STEFANSKA, Barbara</au><au>CHEISHVILI, David</au><au>RAQIB, Rubhana</au><au>TANVIR, Imrana</au><au>HASEEB AHMED KHAN</au><au>RABBANI, Shafaat A</au><au>SZYF, Moshe</au><au>SUDERMAN, Matthew</au><au>ARAKELIAN, Ani</au><au>JIAN HUANG</au><au>HALLETT, Michael</au><au>HAN, Ze-Guang</au><au>AL-MAHTAB, Mamun</au><au>SHEIKH MOHAMMAD FAZLE AKBAR</au><au>WASIF ALI KHAN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-Wide Study of Hypomethylated and Induced Genes in Patients with Liver Cancer Unravels Novel Anticancer Targets</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2014-06-15</date><risdate>2014</risdate><volume>20</volume><issue>12</issue><spage>3118</spage><epage>3132</epage><pages>3118-3132</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><coden>CCREF4</coden><abstract>We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.
We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.
Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>24763612</pmid><doi>10.1158/1078-0432.CCR-13-0283</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2014-06, Vol.20 (12), p.3118-3132 |
| issn | 1078-0432 1557-3265 |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic agents Biological and medical sciences Biomarkers, Tumor - genetics Carcinoma, Hepatocellular - genetics Carrier Proteins - antagonists & inhibitors Carrier Proteins - genetics Cell Movement Cell Proliferation Cysteine Endopeptidases - chemistry Cysteine Endopeptidases - genetics DNA Methylation Exosome Multienzyme Ribonuclease Complex - antagonists & inhibitors Exosome Multienzyme Ribonuclease Complex - genetics Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Regulation, Neoplastic Genome-Wide Association Study Humans Intercellular Signaling Peptides and Proteins - genetics Liver Neoplasms - genetics Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Methyltransferases - antagonists & inhibitors Methyltransferases - genetics Mice Mice, Inbred NOD Mice, SCID Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Nerve Tissue Proteins - genetics Pharmacology. Drug treatments Promoter Regions, Genetic - genetics RNA, Small Interfering - genetics RNA-Binding Proteins - antagonists & inhibitors RNA-Binding Proteins - genetics Signal Transduction Tumors |
| title | Genome-Wide Study of Hypomethylated and Induced Genes in Patients with Liver Cancer Unravels Novel Anticancer Targets |
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