BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells
Bcl-2-associated transcription factor 1 (BCLAF1) is known to be involved in multiple biological processes. Although several splice variants of BCLAF1 have been identified, little is known about how BCLAF1 splicing is regulated or the contribution of alternative splicing to its developmental function...
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| Veröffentlicht in: | Nature communications 2014-08, Vol.5 (1), p.4581-4581, Article 4581 |
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| creator | Zhou, Xuexia Li, Xuebing Cheng, Yuanming Wu, Wenwu Xie, Zhiqin Xi, Qiulei Han, Jun Wu, Guohao Fang, Jing Feng, Ying |
| description | Bcl-2-associated transcription factor 1 (BCLAF1) is known to be involved in multiple biological processes. Although several splice variants of BCLAF1 have been identified, little is known about how BCLAF1 splicing is regulated or the contribution of alternative splicing to its developmental functions. Here we find that inclusion of alternative exon5a was significantly increased in colorectal cancer (CRC) samples. Knockdown of the BCLAF1 protein isoform resulting from exon5a inclusion inhibited growth and that its overexpression increased tumorigenic potential. We also found that the splicing factor SRSF10 stimulates inclusion of exon5a and has growth-inducing activity. Importantly, the upregulation of SRSF10 expression observed in clinical CRC samples parallels the increased inclusion of
BCLAF1
exon5a, both of which are associated with higher tumour grade. These findings identify SRSF10 as a key regulator of BCLAF1 pre-mRNA splicing and the maintenance of oncogenic features in human colon cancer cells.
Alternative splicing often alters the biological function of proteins. Here, Zhou
et al
. show that the splicing factor SRSF10 directs the inclusion of exon5a in Bcl-2-associated transcription factor 1, and that this drives cell growth and tumorigenic potential in human colon cancer cells. |
| doi_str_mv | 10.1038/ncomms5581 |
| format | Article |
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BCLAF1
exon5a, both of which are associated with higher tumour grade. These findings identify SRSF10 as a key regulator of BCLAF1 pre-mRNA splicing and the maintenance of oncogenic features in human colon cancer cells.
Alternative splicing often alters the biological function of proteins. Here, Zhou
et al
. show that the splicing factor SRSF10 directs the inclusion of exon5a in Bcl-2-associated transcription factor 1, and that this drives cell growth and tumorigenic potential in human colon cancer cells.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms5581</identifier><identifier>PMID: 25091051</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/106 ; 13/44 ; 38/109 ; 38/61 ; 38/71 ; 38/90 ; 631/337/1645/1792 ; 631/67/1504/1885/1393 ; 692/420/755 ; Alternative Splicing ; Animals ; Antineoplastic Agents - chemistry ; Carcinoma - genetics ; Carcinoma - metabolism ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Colonic Neoplasms - genetics ; Colonic Neoplasms - metabolism ; Colorectal cancer ; Exons ; Food safety ; Gene Expression Regulation, Neoplastic ; Humanities and Social Sciences ; Humans ; Kinases ; Lung cancer ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mice, Nude ; multidisciplinary ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; Proteins ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; RNA Precursors - genetics ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Science ; Science (multidisciplinary) ; Serine-Arginine Splicing Factors ; Transcription factors ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Tumorigenesis ; Up-Regulation</subject><ispartof>Nature communications, 2014-08, Vol.5 (1), p.4581-4581, Article 4581</ispartof><rights>Springer Nature Limited 2014</rights><rights>Copyright Nature Publishing Group Aug 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-3fb1baf67b23c5864ecc776ab5ac616a998674f8b3cfe591131d2f0da104a8413</citedby><cites>FETCH-LOGICAL-c387t-3fb1baf67b23c5864ecc776ab5ac616a998674f8b3cfe591131d2f0da104a8413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ncomms5581$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://doi.org/10.1038/ncomms5581$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41096,42165,51551</link.rule.ids><linktorsrc>$$Uhttps://doi.org/10.1038/ncomms5581$$EView_record_in_Springer_Nature$$FView_record_in_$$GSpringer_Nature</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25091051$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Xuexia</creatorcontrib><creatorcontrib>Li, Xuebing</creatorcontrib><creatorcontrib>Cheng, Yuanming</creatorcontrib><creatorcontrib>Wu, Wenwu</creatorcontrib><creatorcontrib>Xie, Zhiqin</creatorcontrib><creatorcontrib>Xi, Qiulei</creatorcontrib><creatorcontrib>Han, Jun</creatorcontrib><creatorcontrib>Wu, Guohao</creatorcontrib><creatorcontrib>Fang, Jing</creatorcontrib><creatorcontrib>Feng, Ying</creatorcontrib><title>BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Bcl-2-associated transcription factor 1 (BCLAF1) is known to be involved in multiple biological processes. Although several splice variants of BCLAF1 have been identified, little is known about how BCLAF1 splicing is regulated or the contribution of alternative splicing to its developmental functions. Here we find that inclusion of alternative exon5a was significantly increased in colorectal cancer (CRC) samples. Knockdown of the BCLAF1 protein isoform resulting from exon5a inclusion inhibited growth and that its overexpression increased tumorigenic potential. We also found that the splicing factor SRSF10 stimulates inclusion of exon5a and has growth-inducing activity. Importantly, the upregulation of SRSF10 expression observed in clinical CRC samples parallels the increased inclusion of
BCLAF1
exon5a, both of which are associated with higher tumour grade. These findings identify SRSF10 as a key regulator of BCLAF1 pre-mRNA splicing and the maintenance of oncogenic features in human colon cancer cells.
Alternative splicing often alters the biological function of proteins. Here, Zhou
et al
. show that the splicing factor SRSF10 directs the inclusion of exon5a in Bcl-2-associated transcription factor 1, and that this drives cell growth and tumorigenic potential in human colon cancer cells.</description><subject>13</subject><subject>13/106</subject><subject>13/44</subject><subject>38/109</subject><subject>38/61</subject><subject>38/71</subject><subject>38/90</subject><subject>631/337/1645/1792</subject><subject>631/67/1504/1885/1393</subject><subject>692/420/755</subject><subject>Alternative Splicing</subject><subject>Animals</subject><subject>Antineoplastic Agents - chemistry</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Colonic Neoplasms - genetics</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colorectal cancer</subject><subject>Exons</subject><subject>Food safety</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Mice, Nude</subject><subject>multidisciplinary</subject><subject>Neoplasm Transplantation</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Proteins</subject><subject>Repressor Proteins - 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Academic</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Zhou, Xuexia</au><au>Li, Xuebing</au><au>Cheng, Yuanming</au><au>Wu, Wenwu</au><au>Xie, Zhiqin</au><au>Xi, Qiulei</au><au>Han, Jun</au><au>Wu, Guohao</au><au>Fang, Jing</au><au>Feng, Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-08-05</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>4581</spage><epage>4581</epage><pages>4581-4581</pages><artnum>4581</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Bcl-2-associated transcription factor 1 (BCLAF1) is known to be involved in multiple biological processes. Although several splice variants of BCLAF1 have been identified, little is known about how BCLAF1 splicing is regulated or the contribution of alternative splicing to its developmental functions. Here we find that inclusion of alternative exon5a was significantly increased in colorectal cancer (CRC) samples. Knockdown of the BCLAF1 protein isoform resulting from exon5a inclusion inhibited growth and that its overexpression increased tumorigenic potential. We also found that the splicing factor SRSF10 stimulates inclusion of exon5a and has growth-inducing activity. Importantly, the upregulation of SRSF10 expression observed in clinical CRC samples parallels the increased inclusion of
BCLAF1
exon5a, both of which are associated with higher tumour grade. These findings identify SRSF10 as a key regulator of BCLAF1 pre-mRNA splicing and the maintenance of oncogenic features in human colon cancer cells.
Alternative splicing often alters the biological function of proteins. Here, Zhou
et al
. show that the splicing factor SRSF10 directs the inclusion of exon5a in Bcl-2-associated transcription factor 1, and that this drives cell growth and tumorigenic potential in human colon cancer cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25091051</pmid><doi>10.1038/ncomms5581</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/106 13/44 38/109 38/61 38/71 38/90 631/337/1645/1792 631/67/1504/1885/1393 692/420/755 Alternative Splicing Animals Antineoplastic Agents - chemistry Carcinoma - genetics Carcinoma - metabolism Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell growth Cell Line, Tumor Cell Proliferation Colonic Neoplasms - genetics Colonic Neoplasms - metabolism Colorectal cancer Exons Food safety Gene Expression Regulation, Neoplastic Humanities and Social Sciences Humans Kinases Lung cancer Male Mice Mice, Inbred BALB C Mice, Knockout Mice, Nude multidisciplinary Neoplasm Transplantation Oligonucleotide Array Sequence Analysis Proteins Repressor Proteins - genetics Repressor Proteins - metabolism RNA Precursors - genetics RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Science Science (multidisciplinary) Serine-Arginine Splicing Factors Transcription factors Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Tumorigenesis Up-Regulation |
| title | BCLAF1 and its splicing regulator SRSF10 regulate the tumorigenic potential of colon cancer cells |
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