Expression of RASSF1A, an epigenetically silenced tumor suppressor, overcomes resistance to apoptosis induction by interferons
Resistance of human renal cell carcinoma (RCC) and melanoma to the apoptosis-inducing effects of IFNs was postulated to result from epigenetic silencing of genes by DNA methylation, a common feature of human cancers. To reverse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2006-03, Vol.66 (5), p.2785-2793 |
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| creator | REU, Frederic J LEAMAN, Douglas W MAITRA, Ratan R SOO IN BAE CHERKASSKY, Leonid FOX, Mark W REMPINSKI, Donald R BEAULIEU, Normand MACLEOD, A. Robert BORDEN, Ernest C |
| description | Resistance of human renal cell carcinoma (RCC) and melanoma to the apoptosis-inducing effects of IFNs was postulated to result from epigenetic silencing of genes by DNA methylation, a common feature of human cancers. To reverse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA methyltransferase 1 (DNMT1) by phosphorothioate oligonucleotide antisense (DNMT1 AS) were employed in cells resistant (400-fold higher TRAIL decoy receptor 1 expression than transduced ACHN cells (real-time reverse transcription-PCR). Results identified RASSF1A as regulated by IFNs and participating in IFN-induced apoptosis at least in part by sensitization to TRAIL. |
| doi_str_mv | 10.1158/0008-5472.CAN-05-2303 |
| format | Article |
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Robert ; BORDEN, Ernest C</creator><creatorcontrib>REU, Frederic J ; LEAMAN, Douglas W ; MAITRA, Ratan R ; SOO IN BAE ; CHERKASSKY, Leonid ; FOX, Mark W ; REMPINSKI, Donald R ; BEAULIEU, Normand ; MACLEOD, A. Robert ; BORDEN, Ernest C</creatorcontrib><description>Resistance of human renal cell carcinoma (RCC) and melanoma to the apoptosis-inducing effects of IFNs was postulated to result from epigenetic silencing of genes by DNA methylation, a common feature of human cancers. To reverse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA methyltransferase 1 (DNMT1) by phosphorothioate oligonucleotide antisense (DNMT1 AS) were employed in cells resistant (<5% terminal deoxynucleotidyl transferase-mediated nick-end labeling positive) to apoptosis induction by IFN-alpha2 and IFN-beta (ACHN, SK-RC-45, and A375). 5-AZA-dC and DNMT1 AS similarly depleted available DNMT1 protein and, at doses that did not cause apoptosis alone, resulted in apoptotic response to IFNs. The proapoptotic tumor suppressor RASSF1A was reactivated by DNMT1 inhibitors in all three cell lines. This was associated with demethylation of its promoter region. IFNs augmented RASSF1A protein expression after reactivation by DNMT1 inhibition. In IFN-sensitive WM9 melanoma cells, expression of RASSF1A was constitutive but also augmented by IFNs. RASSF1A small interfering RNA reduced IFN-induced apoptosis in WM9 cells and in DNMT1-depleted ACHN cells. Conversely, lentiviral expression of RASSF1A but not transduction with empty virus enabled IFN-induced apoptosis. IFN induced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL-neutralizing antibody inhibited apoptotic response to IFN in RASSF1A-expressing ACHN cells. Accordingly, RASSF1A markedly sensitized to recombinant TRAIL. Normal kidney epithelial cells, although expressing RASSF1A, did not undergo apoptosis in response to IFN or TRAIL but had >400-fold higher TRAIL decoy receptor 1 expression than transduced ACHN cells (real-time reverse transcription-PCR). Results identified RASSF1A as regulated by IFNs and participating in IFN-induced apoptosis at least in part by sensitization to TRAIL.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>DOI: 10.1158/0008-5472.CAN-05-2303</identifier><identifier>PMID: 16510600</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Antineoplastic agents ; Apoptosis - drug effects ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - pharmacology ; Biological and medical sciences ; Carcinoma, Renal Cell - drug therapy ; Carcinoma, Renal Cell - genetics ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - pathology ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors ; DNA (Cytosine-5-)-Methyltransferases - deficiency ; Drug Resistance, Neoplasm ; Epigenesis, Genetic ; Gene Silencing ; HeLa Cells ; Humans ; Interferon-alpha - pharmacology ; Interferon-beta - pharmacology ; Kidney Neoplasms - drug therapy ; Kidney Neoplasms - genetics ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Lentivirus - genetics ; Lentivirus - metabolism ; Medical sciences ; Melanoma - drug therapy ; Melanoma - genetics ; Melanoma - metabolism ; Melanoma - pathology ; Membrane Glycoproteins - pharmacology ; Pharmacology. Drug treatments ; Promoter Regions, Genetic ; RNA, Small Interfering - genetics ; TNF-Related Apoptosis-Inducing Ligand ; Transfection ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor Suppressor Proteins - antagonists & inhibitors ; Tumor Suppressor Proteins - biosynthesis ; Tumor Suppressor Proteins - genetics ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 2006-03, Vol.66 (5), p.2785-2793</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-8b687fd0898cebc044d89897706a2a34cb1307dc730f8f26812a476a7a49dee63</citedby><cites>FETCH-LOGICAL-c503t-8b687fd0898cebc044d89897706a2a34cb1307dc730f8f26812a476a7a49dee63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17572721$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16510600$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>REU, Frederic J</creatorcontrib><creatorcontrib>LEAMAN, Douglas W</creatorcontrib><creatorcontrib>MAITRA, Ratan R</creatorcontrib><creatorcontrib>SOO IN BAE</creatorcontrib><creatorcontrib>CHERKASSKY, Leonid</creatorcontrib><creatorcontrib>FOX, Mark W</creatorcontrib><creatorcontrib>REMPINSKI, Donald R</creatorcontrib><creatorcontrib>BEAULIEU, Normand</creatorcontrib><creatorcontrib>MACLEOD, A. Robert</creatorcontrib><creatorcontrib>BORDEN, Ernest C</creatorcontrib><title>Expression of RASSF1A, an epigenetically silenced tumor suppressor, overcomes resistance to apoptosis induction by interferons</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Resistance of human renal cell carcinoma (RCC) and melanoma to the apoptosis-inducing effects of IFNs was postulated to result from epigenetic silencing of genes by DNA methylation, a common feature of human cancers. To reverse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA methyltransferase 1 (DNMT1) by phosphorothioate oligonucleotide antisense (DNMT1 AS) were employed in cells resistant (<5% terminal deoxynucleotidyl transferase-mediated nick-end labeling positive) to apoptosis induction by IFN-alpha2 and IFN-beta (ACHN, SK-RC-45, and A375). 5-AZA-dC and DNMT1 AS similarly depleted available DNMT1 protein and, at doses that did not cause apoptosis alone, resulted in apoptotic response to IFNs. The proapoptotic tumor suppressor RASSF1A was reactivated by DNMT1 inhibitors in all three cell lines. This was associated with demethylation of its promoter region. IFNs augmented RASSF1A protein expression after reactivation by DNMT1 inhibition. In IFN-sensitive WM9 melanoma cells, expression of RASSF1A was constitutive but also augmented by IFNs. RASSF1A small interfering RNA reduced IFN-induced apoptosis in WM9 cells and in DNMT1-depleted ACHN cells. Conversely, lentiviral expression of RASSF1A but not transduction with empty virus enabled IFN-induced apoptosis. IFN induced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL-neutralizing antibody inhibited apoptotic response to IFN in RASSF1A-expressing ACHN cells. Accordingly, RASSF1A markedly sensitized to recombinant TRAIL. Normal kidney epithelial cells, although expressing RASSF1A, did not undergo apoptosis in response to IFN or TRAIL but had >400-fold higher TRAIL decoy receptor 1 expression than transduced ACHN cells (real-time reverse transcription-PCR). Results identified RASSF1A as regulated by IFNs and participating in IFN-induced apoptosis at least in part by sensitization to TRAIL.</description><subject>Antineoplastic agents</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Renal Cell - drug therapy</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Carcinoma, Renal Cell - metabolism</subject><subject>Carcinoma, Renal Cell - pathology</subject><subject>DNA (Cytosine-5-)-Methyltransferase 1</subject><subject>DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors</subject><subject>DNA (Cytosine-5-)-Methyltransferases - deficiency</subject><subject>Drug Resistance, Neoplasm</subject><subject>Epigenesis, Genetic</subject><subject>Gene Silencing</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Interferon-alpha - pharmacology</subject><subject>Interferon-beta - pharmacology</subject><subject>Kidney Neoplasms - drug therapy</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Lentivirus - genetics</subject><subject>Lentivirus - metabolism</subject><subject>Medical sciences</subject><subject>Melanoma - drug therapy</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Membrane Glycoproteins - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Promoter Regions, Genetic</subject><subject>RNA, Small Interfering - genetics</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>Transfection</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor Suppressor Proteins - antagonists & inhibitors</subject><subject>Tumor Suppressor Proteins - biosynthesis</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQQC0EosvCTwD5Qk9NsePPXJBWqxaQKpAonC3HmRSjJA62U7EXfjsOXbVw4uSZ8ZsZWw-hl5ScUyr0G0KIrgRX9fl-97EioqoZYY_QhgqmK8W5eIw298wJepbS95IKSsRTdEJlCSQhG_Tr4uccISUfJhx6_Hl3fX1Jd2fYThhmfwMTZO_sMBxw8gNMDjqclzFEnJb5T2OIZzjcQnRhhIRLxadsC4dzwHYOcw6lgv3ULS6vS9pDSTLEHmKY0nP0pLdDghfHc4u-Xl582b-vrj69-7DfXVVOEJYr3Uqt-o7oRjtoHeG8K2GjFJG2toy7ljKiOqcY6XVfS01ry5W0yvKmA5Bsi97ezZ2XdoTOwZSjHcwc_WjjwQTrzb83k_9mbsKtoUo2QtAy4PQ4IIYfC6RsRp8cDIOdICzJSKUop-z_IG00Y6K42iJxB7oYUorQ37-GErMqNqs-s-ozRbEhwqyKS9-rv7_y0HV0WoDXR8Cmoq6PRYdPD5wSqlY1Zb8BN9eySQ</recordid><startdate>20060301</startdate><enddate>20060301</enddate><creator>REU, Frederic J</creator><creator>LEAMAN, Douglas W</creator><creator>MAITRA, Ratan R</creator><creator>SOO IN BAE</creator><creator>CHERKASSKY, Leonid</creator><creator>FOX, Mark W</creator><creator>REMPINSKI, Donald R</creator><creator>BEAULIEU, Normand</creator><creator>MACLEOD, A. Robert</creator><creator>BORDEN, Ernest C</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060301</creationdate><title>Expression of RASSF1A, an epigenetically silenced tumor suppressor, overcomes resistance to apoptosis induction by interferons</title><author>REU, Frederic J ; LEAMAN, Douglas W ; MAITRA, Ratan R ; SOO IN BAE ; CHERKASSKY, Leonid ; FOX, Mark W ; REMPINSKI, Donald R ; BEAULIEU, Normand ; MACLEOD, A. Robert ; BORDEN, Ernest C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-8b687fd0898cebc044d89897706a2a34cb1307dc730f8f26812a476a7a49dee63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Antineoplastic agents</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Renal Cell - drug therapy</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Carcinoma, Renal Cell - metabolism</topic><topic>Carcinoma, Renal Cell - pathology</topic><topic>DNA (Cytosine-5-)-Methyltransferase 1</topic><topic>DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors</topic><topic>DNA (Cytosine-5-)-Methyltransferases - deficiency</topic><topic>Drug Resistance, Neoplasm</topic><topic>Epigenesis, Genetic</topic><topic>Gene Silencing</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Interferon-alpha - pharmacology</topic><topic>Interferon-beta - pharmacology</topic><topic>Kidney Neoplasms - drug therapy</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - metabolism</topic><topic>Kidney Neoplasms - pathology</topic><topic>Lentivirus - genetics</topic><topic>Lentivirus - metabolism</topic><topic>Medical sciences</topic><topic>Melanoma - drug therapy</topic><topic>Melanoma - genetics</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - pathology</topic><topic>Membrane Glycoproteins - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Promoter Regions, Genetic</topic><topic>RNA, Small Interfering - genetics</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>Transfection</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor Suppressor Proteins - antagonists & inhibitors</topic><topic>Tumor Suppressor Proteins - biosynthesis</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>REU, Frederic J</creatorcontrib><creatorcontrib>LEAMAN, Douglas W</creatorcontrib><creatorcontrib>MAITRA, Ratan R</creatorcontrib><creatorcontrib>SOO IN BAE</creatorcontrib><creatorcontrib>CHERKASSKY, Leonid</creatorcontrib><creatorcontrib>FOX, Mark W</creatorcontrib><creatorcontrib>REMPINSKI, Donald R</creatorcontrib><creatorcontrib>BEAULIEU, Normand</creatorcontrib><creatorcontrib>MACLEOD, A. 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Robert</au><au>BORDEN, Ernest C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of RASSF1A, an epigenetically silenced tumor suppressor, overcomes resistance to apoptosis induction by interferons</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>2006-03-01</date><risdate>2006</risdate><volume>66</volume><issue>5</issue><spage>2785</spage><epage>2793</epage><pages>2785-2793</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Resistance of human renal cell carcinoma (RCC) and melanoma to the apoptosis-inducing effects of IFNs was postulated to result from epigenetic silencing of genes by DNA methylation, a common feature of human cancers. To reverse silencing, 5-AZA-deoxycytidine (5-AZA-dC) or selective depletion of DNA methyltransferase 1 (DNMT1) by phosphorothioate oligonucleotide antisense (DNMT1 AS) were employed in cells resistant (<5% terminal deoxynucleotidyl transferase-mediated nick-end labeling positive) to apoptosis induction by IFN-alpha2 and IFN-beta (ACHN, SK-RC-45, and A375). 5-AZA-dC and DNMT1 AS similarly depleted available DNMT1 protein and, at doses that did not cause apoptosis alone, resulted in apoptotic response to IFNs. The proapoptotic tumor suppressor RASSF1A was reactivated by DNMT1 inhibitors in all three cell lines. This was associated with demethylation of its promoter region. IFNs augmented RASSF1A protein expression after reactivation by DNMT1 inhibition. In IFN-sensitive WM9 melanoma cells, expression of RASSF1A was constitutive but also augmented by IFNs. RASSF1A small interfering RNA reduced IFN-induced apoptosis in WM9 cells and in DNMT1-depleted ACHN cells. Conversely, lentiviral expression of RASSF1A but not transduction with empty virus enabled IFN-induced apoptosis. IFN induced tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL-neutralizing antibody inhibited apoptotic response to IFN in RASSF1A-expressing ACHN cells. Accordingly, RASSF1A markedly sensitized to recombinant TRAIL. Normal kidney epithelial cells, although expressing RASSF1A, did not undergo apoptosis in response to IFN or TRAIL but had >400-fold higher TRAIL decoy receptor 1 expression than transduced ACHN cells (real-time reverse transcription-PCR). Results identified RASSF1A as regulated by IFNs and participating in IFN-induced apoptosis at least in part by sensitization to TRAIL.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>16510600</pmid><doi>10.1158/0008-5472.CAN-05-2303</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 2006-03, Vol.66 (5), p.2785-2793 |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Antineoplastic agents Apoptosis - drug effects Apoptosis - genetics Apoptosis Regulatory Proteins - pharmacology Biological and medical sciences Carcinoma, Renal Cell - drug therapy Carcinoma, Renal Cell - genetics Carcinoma, Renal Cell - metabolism Carcinoma, Renal Cell - pathology DNA (Cytosine-5-)-Methyltransferase 1 DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors DNA (Cytosine-5-)-Methyltransferases - deficiency Drug Resistance, Neoplasm Epigenesis, Genetic Gene Silencing HeLa Cells Humans Interferon-alpha - pharmacology Interferon-beta - pharmacology Kidney Neoplasms - drug therapy Kidney Neoplasms - genetics Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Lentivirus - genetics Lentivirus - metabolism Medical sciences Melanoma - drug therapy Melanoma - genetics Melanoma - metabolism Melanoma - pathology Membrane Glycoproteins - pharmacology Pharmacology. Drug treatments Promoter Regions, Genetic RNA, Small Interfering - genetics TNF-Related Apoptosis-Inducing Ligand Transfection Tumor Necrosis Factor-alpha - pharmacology Tumor Suppressor Proteins - antagonists & inhibitors Tumor Suppressor Proteins - biosynthesis Tumor Suppressor Proteins - genetics Tumors |
| title | Expression of RASSF1A, an epigenetically silenced tumor suppressor, overcomes resistance to apoptosis induction by interferons |
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