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Targeting ARID1A-mutant colorectal cancer: depletion of ARID1B increases radiosensitivity and modulates DNA damage response
The SWI/SNF chromatin remodeling complex has been found mutated in a wide range of human cancers, causing alterations in gene expression patterns, proliferation and DNA damage response that have been linked to poor clinical prognosis. Here, we investigated weather knockdown of ARID1B, one of two mut...
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| Published in: | Scientific reports 2019-12, Vol.9 (1), p.18207-9, Article 18207 |
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| description | The SWI/SNF chromatin remodeling complex has been found mutated in a wide range of human cancers, causing alterations in gene expression patterns, proliferation and DNA damage response that have been linked to poor clinical prognosis. Here, we investigated weather knockdown of ARID1B, one of two mutually exclusive subunits within the SWI/SNF complex, can sensitize colorectal cancer cell lines mutated in the other subunit, ARID1A, to ionizing radiation (IR). ARID1A-mutated colorectal cancer (CRC) cell lines are selectively sensitized to IR after siRNA mediated ARID1B depletion, as measured by clonogenic survival. This is characterized by a decrease in the surviving cell fraction to 87.3% ± 2.1%, 86.0% ± 1.1% and 77.2% ± 1.5% per 1 Gy compared with control siRNA exposed cells in the dose range of 0-6 Gy for the LS180, RKO and SW48 lines, respectively (p |
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Here, we investigated weather knockdown of ARID1B, one of two mutually exclusive subunits within the SWI/SNF complex, can sensitize colorectal cancer cell lines mutated in the other subunit, ARID1A, to ionizing radiation (IR). ARID1A-mutated colorectal cancer (CRC) cell lines are selectively sensitized to IR after siRNA mediated ARID1B depletion, as measured by clonogenic survival. This is characterized by a decrease in the surviving cell fraction to 87.3% ± 2.1%, 86.0% ± 1.1% and 77.2% ± 1.5% per 1 Gy compared with control siRNA exposed cells in the dose range of 0-6 Gy for the LS180, RKO and SW48 lines, respectively (p < 0.0001, F-test). The magnitude of this dose modifying effect was significantly larger in ARID1A mutated than in non-mutated cell lines (Spearman rank correlation rs = 0.88, p = 0.02). Furthermore, initial formation of RAD51 foci at 4 h after IR, as a measure for homologous recombination repair, was significantly reduced in ARID1A-mutant CRC cell lines but not in the majority of wildtype lines nor in fibroblasts. These findings open up perspectives for targeting ARID1B in combination with radiotherapy to improve outcomes of patients with ARID1A-mutant CRC.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-54757-z</identifier><identifier>PMID: 31796878</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Cancer ; Cell Line, Tumor ; Chemoradiotherapy - methods ; Chromatin Assembly and Disassembly - drug effects ; Chromatin Assembly and Disassembly - genetics ; Chromatin Assembly and Disassembly - radiation effects ; Chromatin remodeling ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - therapy ; Deoxyribonucleic acid ; DNA ; DNA Breaks, Double-Stranded - radiation effects ; DNA damage ; DNA Repair - drug effects ; DNA Repair - genetics ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - genetics ; Fibroblasts ; Gene expression ; Gene Knockdown Techniques ; Homologous recombination ; Homologous recombination repair ; Humans ; Ionizing radiation ; Medical prognosis ; Mutation ; Rad51 Recombinase - metabolism ; Radiation therapy ; Radiation Tolerance - genetics ; Radiosensitivity ; RNA, Small Interfering - metabolism ; siRNA ; SWI/SNF complex ; Transcription Factors - antagonists & inhibitors ; Transcription Factors - genetics ; Tumor cell lines ; Tumor Stem Cell Assay ; Tumor Suppressor p53-Binding Protein 1 - metabolism</subject><ispartof>Scientific reports, 2019-12, Vol.9 (1), p.18207-9, Article 18207</ispartof><rights>2019. 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Here, we investigated weather knockdown of ARID1B, one of two mutually exclusive subunits within the SWI/SNF complex, can sensitize colorectal cancer cell lines mutated in the other subunit, ARID1A, to ionizing radiation (IR). ARID1A-mutated colorectal cancer (CRC) cell lines are selectively sensitized to IR after siRNA mediated ARID1B depletion, as measured by clonogenic survival. This is characterized by a decrease in the surviving cell fraction to 87.3% ± 2.1%, 86.0% ± 1.1% and 77.2% ± 1.5% per 1 Gy compared with control siRNA exposed cells in the dose range of 0-6 Gy for the LS180, RKO and SW48 lines, respectively (p < 0.0001, F-test). The magnitude of this dose modifying effect was significantly larger in ARID1A mutated than in non-mutated cell lines (Spearman rank correlation rs = 0.88, p = 0.02). Furthermore, initial formation of RAD51 foci at 4 h after IR, as a measure for homologous recombination repair, was significantly reduced in ARID1A-mutant CRC cell lines but not in the majority of wildtype lines nor in fibroblasts. These findings open up perspectives for targeting ARID1B in combination with radiotherapy to improve outcomes of patients with ARID1A-mutant CRC.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Chemoradiotherapy - methods</subject><subject>Chromatin Assembly and Disassembly - drug effects</subject><subject>Chromatin Assembly and Disassembly - genetics</subject><subject>Chromatin Assembly and Disassembly - radiation effects</subject><subject>Chromatin remodeling</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - therapy</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Breaks, Double-Stranded - radiation effects</subject><subject>DNA damage</subject><subject>DNA Repair - drug effects</subject><subject>DNA Repair - 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metabolism</topic><topic>Radiation therapy</topic><topic>Radiation Tolerance - genetics</topic><topic>Radiosensitivity</topic><topic>RNA, Small Interfering - metabolism</topic><topic>siRNA</topic><topic>SWI/SNF complex</topic><topic>Transcription Factors - antagonists & inhibitors</topic><topic>Transcription Factors - genetics</topic><topic>Tumor cell lines</topic><topic>Tumor Stem Cell Assay</topic><topic>Tumor Suppressor p53-Binding Protein 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Niedermaier, B</creatorcontrib><creatorcontrib>Sak, A</creatorcontrib><creatorcontrib>Zernickel, E</creatorcontrib><creatorcontrib>Xu, Shan</creatorcontrib><creatorcontrib>Groneberg, M</creatorcontrib><creatorcontrib>Stuschke, M</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>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Niedermaier, B</au><au>Sak, A</au><au>Zernickel, E</au><au>Xu, Shan</au><au>Groneberg, M</au><au>Stuschke, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting ARID1A-mutant colorectal cancer: depletion of ARID1B increases radiosensitivity and modulates DNA damage response</atitle><jtitle>Scientific reports</jtitle><addtitle>Sci Rep</addtitle><date>2019-12-03</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>18207</spage><epage>9</epage><pages>18207-9</pages><artnum>18207</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>The SWI/SNF chromatin remodeling complex has been found mutated in a wide range of human cancers, causing alterations in gene expression patterns, proliferation and DNA damage response that have been linked to poor clinical prognosis. Here, we investigated weather knockdown of ARID1B, one of two mutually exclusive subunits within the SWI/SNF complex, can sensitize colorectal cancer cell lines mutated in the other subunit, ARID1A, to ionizing radiation (IR). ARID1A-mutated colorectal cancer (CRC) cell lines are selectively sensitized to IR after siRNA mediated ARID1B depletion, as measured by clonogenic survival. This is characterized by a decrease in the surviving cell fraction to 87.3% ± 2.1%, 86.0% ± 1.1% and 77.2% ± 1.5% per 1 Gy compared with control siRNA exposed cells in the dose range of 0-6 Gy for the LS180, RKO and SW48 lines, respectively (p < 0.0001, F-test). The magnitude of this dose modifying effect was significantly larger in ARID1A mutated than in non-mutated cell lines (Spearman rank correlation rs = 0.88, p = 0.02). Furthermore, initial formation of RAD51 foci at 4 h after IR, as a measure for homologous recombination repair, was significantly reduced in ARID1A-mutant CRC cell lines but not in the majority of wildtype lines nor in fibroblasts. These findings open up perspectives for targeting ARID1B in combination with radiotherapy to improve outcomes of patients with ARID1A-mutant CRC.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>31796878</pmid><doi>10.1038/s41598-019-54757-z</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Cancer Cell Line, Tumor Chemoradiotherapy - methods Chromatin Assembly and Disassembly - drug effects Chromatin Assembly and Disassembly - genetics Chromatin Assembly and Disassembly - radiation effects Chromatin remodeling Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - therapy Deoxyribonucleic acid DNA DNA Breaks, Double-Stranded - radiation effects DNA damage DNA Repair - drug effects DNA Repair - genetics DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - genetics Fibroblasts Gene expression Gene Knockdown Techniques Homologous recombination Homologous recombination repair Humans Ionizing radiation Medical prognosis Mutation Rad51 Recombinase - metabolism Radiation therapy Radiation Tolerance - genetics Radiosensitivity RNA, Small Interfering - metabolism siRNA SWI/SNF complex Transcription Factors - antagonists & inhibitors Transcription Factors - genetics Tumor cell lines Tumor Stem Cell Assay Tumor Suppressor p53-Binding Protein 1 - metabolism |
| title | Targeting ARID1A-mutant colorectal cancer: depletion of ARID1B increases radiosensitivity and modulates DNA damage response |
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