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Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development
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| Zeitschriftentitel: | Molecular Cancer Research |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , |
| In: | Molecular Cancer Research, 12, 2014, 4, S. 560-570 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
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| Schlagwörter: |
| author_facet |
Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. |
|---|---|
| author |
Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. |
| spellingShingle |
Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. Molecular Cancer Research Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development Cancer Research Oncology Molecular Biology |
| author_sort |
song, shujie |
| spelling |
Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-13-0427 <jats:title>Abstract</jats:title> <jats:p>The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non–small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development.</jats:p> <jats:p>Implications: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development. Mol Cancer Res; 12(4); 560–70. ©2014 AACR.</jats:p> Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development Molecular Cancer Research |
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| title |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_unstemmed |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_full |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_fullStr |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_full_unstemmed |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_short |
Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_sort |
gene silencing associated with swi/snf complex loss during nsclc development |
| topic |
Cancer Research Oncology Molecular Biology |
| url |
http://dx.doi.org/10.1158/1541-7786.mcr-13-0427 |
| publishDate |
2014 |
| physical |
560-570 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non–small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development.</jats:p>
<jats:p>Implications: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development. Mol Cancer Res; 12(4); 560–70. ©2014 AACR.</jats:p> |
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| author | Song, Shujie, Walter, Vonn, Karaca, Mehmet, Li, Ying, Bartlett, Christopher S., Smiraglia, Dominic J., Serber, Daniel, Sproul, Christopher D., Plass, Christoph, Zhang, Jiren, Hayes, D. Neil, Zheng, Yanfang, Weissman, Bernard E. |
| author_facet | Song, Shujie, Walter, Vonn, Karaca, Mehmet, Li, Ying, Bartlett, Christopher S., Smiraglia, Dominic J., Serber, Daniel, Sproul, Christopher D., Plass, Christoph, Zhang, Jiren, Hayes, D. Neil, Zheng, Yanfang, Weissman, Bernard E., Song, Shujie, Walter, Vonn, Karaca, Mehmet, Li, Ying, Bartlett, Christopher S., Smiraglia, Dominic J., Serber, Daniel, Sproul, Christopher D., Plass, Christoph, Zhang, Jiren, Hayes, D. Neil, Zheng, Yanfang, Weissman, Bernard E. |
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| description | <jats:title>Abstract</jats:title> <jats:p>The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non–small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development.</jats:p> <jats:p>Implications: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development. Mol Cancer Res; 12(4); 560–70. ©2014 AACR.</jats:p> |
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| imprint_str_mv | American Association for Cancer Research (AACR), 2014 |
| institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Rs1, DE-Pl11, DE-105, DE-14 |
| issn | 1541-7786, 1557-3125 |
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| spelling | Song, Shujie Walter, Vonn Karaca, Mehmet Li, Ying Bartlett, Christopher S. Smiraglia, Dominic J. Serber, Daniel Sproul, Christopher D. Plass, Christoph Zhang, Jiren Hayes, D. Neil Zheng, Yanfang Weissman, Bernard E. 1541-7786 1557-3125 American Association for Cancer Research (AACR) Cancer Research Oncology Molecular Biology http://dx.doi.org/10.1158/1541-7786.mcr-13-0427 <jats:title>Abstract</jats:title> <jats:p>The SWI/SNF chromatin-remodeling complex regulates gene expression and alters chromatin structures in an ATP-dependent manner. Recent sequencing efforts have shown mutations in BRG1 (SMARCA4), one of two mutually exclusive ATPase subunits in the complex, in a significant number of human lung tumor cell lines and primary non–small cell lung carcinoma (NSCLC) clinical specimens. To determine how BRG1 loss fuels tumor progression in NSCLC, molecular profiling was performed after restoration of BRG1 expression or treatment with a histone deacetylase inhibitor or a DNA methyltransferase (DNMT) inhibitor in a BRG1-deficient NSCLC cells. Importantly, validation studies from multiple cell lines revealed that BRG1 reexpression led to substantial changes in the expression of CDH1, CDH3, EHF, and RRAD that commonly undergo silencing by other epigenetic mechanisms during NSCLC development. Furthermore, treatment with DNMT inhibitors did not restore expression of these transcripts, indicating that this common mechanism of gene silencing did not account for their loss of expression. Collectively, BRG1 loss is an important mechanism for the epigenetic silencing of target genes during NSCLC development.</jats:p> <jats:p>Implications: Inactivation of the SWI/SNF complex provides a novel mechanism to induce gene silencing during NSCLC development. Mol Cancer Res; 12(4); 560–70. ©2014 AACR.</jats:p> Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development Molecular Cancer Research |
| spellingShingle | Song, Shujie, Walter, Vonn, Karaca, Mehmet, Li, Ying, Bartlett, Christopher S., Smiraglia, Dominic J., Serber, Daniel, Sproul, Christopher D., Plass, Christoph, Zhang, Jiren, Hayes, D. Neil, Zheng, Yanfang, Weissman, Bernard E., Molecular Cancer Research, Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development, Cancer Research, Oncology, Molecular Biology |
| title | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_full | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_fullStr | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_full_unstemmed | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_short | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| title_sort | gene silencing associated with swi/snf complex loss during nsclc development |
| title_unstemmed | Gene Silencing Associated with SWI/SNF Complex Loss during NSCLC Development |
| topic | Cancer Research, Oncology, Molecular Biology |
| url | http://dx.doi.org/10.1158/1541-7786.mcr-13-0427 |