Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1
Generally shortened 3′ UTR due to alternative polyadenylation (APA) is widely observed in cancer, but its regulation mechanisms for cancer are not well characterized. Here, with profiling of APA in colorectal cancer tissues and poly(A) signal editing, we firstly identified that the shortened 3′ UTR...
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| Veröffentlicht in: | Science China. Life sciences 2024-06, Vol.67 (6), p.1212-1225 |
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| creator | Hu, Zhijie Li, Mengxia Chen, Yufeng Chen, Liutao Han, Yuting Chen, Chengyong Lu, Xin You, Nan Lou, Yawen Huang, Yingye Huo, Zhanfeng Liu, Chao Liang, Cheng Liu, Susu Deng, Ke Chen, Liangfu Chen, Shangwu Wan, Guohui Wu, Xiaojian Fu, Yonggui Xu, Anlong |
| description | Generally shortened 3′ UTR due to alternative polyadenylation (APA) is widely observed in cancer, but its regulation mechanisms for cancer are not well characterized. Here, with profiling of APA in colorectal cancer tissues and poly(A) signal editing, we firstly identified that the shortened 3′ UTR of
CTNNIBP1
in colorectal cancer promotes cell proliferation and migration. We found that liquid-liquid phase separation (LLPS) of PABPN1 is reduced albeit with higher expression in cancer, and the reduction of LLPS leads to the shortened 3′ UTR of
CTNNBIP1
and promotes cell proliferation and migration. Notably, the splicing factor SNRPD2 upregulated in colorectal cancer, can interact with glutamic-proline (EP) domain of PABPN1, and then disrupt LLPS of PABPN1, which attenuates the repression effect of PABPN1 on the proximal poly(A) sites. Our results firstly reveal a new regulation mechanism of APA by disruption of LLPS of PABPN1, suggesting that regulation of APA by interfering LLPS of 3′ end processing factor may have the potential as a new way for the treatment of cancer. |
| doi_str_mv | 10.1007/s11427-023-2495-x |
| format | Article |
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CTNNIBP1
in colorectal cancer promotes cell proliferation and migration. We found that liquid-liquid phase separation (LLPS) of PABPN1 is reduced albeit with higher expression in cancer, and the reduction of LLPS leads to the shortened 3′ UTR of
CTNNBIP1
and promotes cell proliferation and migration. Notably, the splicing factor SNRPD2 upregulated in colorectal cancer, can interact with glutamic-proline (EP) domain of PABPN1, and then disrupt LLPS of PABPN1, which attenuates the repression effect of PABPN1 on the proximal poly(A) sites. Our results firstly reveal a new regulation mechanism of APA by disruption of LLPS of PABPN1, suggesting that regulation of APA by interfering LLPS of 3′ end processing factor may have the potential as a new way for the treatment of cancer.</description><identifier>ISSN: 1674-7305</identifier><identifier>EISSN: 1869-1889</identifier><identifier>DOI: 10.1007/s11427-023-2495-x</identifier><identifier>PMID: 38811444</identifier><language>eng</language><publisher>Beijing: Science China Press</publisher><subject>3' Untranslated regions ; Biomedical and Life Sciences ; Cancer ; Cell growth ; Cell migration ; Cell proliferation ; Colorectal cancer ; Colorectal carcinoma ; Life Sciences ; Polyadenylation ; Reseach Paper ; Splicing factors</subject><ispartof>Science China. Life sciences, 2024-06, Vol.67 (6), p.1212-1225</ispartof><rights>Science China Press 2024</rights><rights>2024. Science China Press.</rights><rights>Science China Press 2024.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c254t-b522eed60c57c80e4a24c8f7f64fe608c4959e7a56eb1160d8785b89761e27953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11427-023-2495-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11427-023-2495-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38811444$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Zhijie</creatorcontrib><creatorcontrib>Li, Mengxia</creatorcontrib><creatorcontrib>Chen, Yufeng</creatorcontrib><creatorcontrib>Chen, Liutao</creatorcontrib><creatorcontrib>Han, Yuting</creatorcontrib><creatorcontrib>Chen, Chengyong</creatorcontrib><creatorcontrib>Lu, Xin</creatorcontrib><creatorcontrib>You, Nan</creatorcontrib><creatorcontrib>Lou, Yawen</creatorcontrib><creatorcontrib>Huang, Yingye</creatorcontrib><creatorcontrib>Huo, Zhanfeng</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Liang, Cheng</creatorcontrib><creatorcontrib>Liu, Susu</creatorcontrib><creatorcontrib>Deng, Ke</creatorcontrib><creatorcontrib>Chen, Liangfu</creatorcontrib><creatorcontrib>Chen, Shangwu</creatorcontrib><creatorcontrib>Wan, Guohui</creatorcontrib><creatorcontrib>Wu, Xiaojian</creatorcontrib><creatorcontrib>Fu, Yonggui</creatorcontrib><creatorcontrib>Xu, Anlong</creatorcontrib><title>Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1</title><title>Science China. Life sciences</title><addtitle>Sci. China Life Sci</addtitle><addtitle>Sci China Life Sci</addtitle><description>Generally shortened 3′ UTR due to alternative polyadenylation (APA) is widely observed in cancer, but its regulation mechanisms for cancer are not well characterized. Here, with profiling of APA in colorectal cancer tissues and poly(A) signal editing, we firstly identified that the shortened 3′ UTR of
CTNNIBP1
in colorectal cancer promotes cell proliferation and migration. We found that liquid-liquid phase separation (LLPS) of PABPN1 is reduced albeit with higher expression in cancer, and the reduction of LLPS leads to the shortened 3′ UTR of
CTNNBIP1
and promotes cell proliferation and migration. Notably, the splicing factor SNRPD2 upregulated in colorectal cancer, can interact with glutamic-proline (EP) domain of PABPN1, and then disrupt LLPS of PABPN1, which attenuates the repression effect of PABPN1 on the proximal poly(A) sites. Our results firstly reveal a new regulation mechanism of APA by disruption of LLPS of PABPN1, suggesting that regulation of APA by interfering LLPS of 3′ end processing factor may have the potential as a new way for the treatment of cancer.</description><subject>3' Untranslated regions</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Life Sciences</subject><subject>Polyadenylation</subject><subject>Reseach Paper</subject><subject>Splicing factors</subject><issn>1674-7305</issn><issn>1869-1889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kU1v1DAQhi0EolXpD-CCLHHhEvC3nWO75aNStaygnCPHmeymcuJgJ1X39_BHcbpbkJCwDx5rnnc84xeh15S8p4ToD4lSwXRBGC-YKGXx8AydUqPKghpTPs-x0qLQnMgTdJ7SHcmLc8K0folOuDFZLcQp-nXVpTiPUxcGHFq8ubjcrCkedzYBTjDaaB9T9R5_X3_bXDHcxO4eEnbBhwhush47OziI2IH3eIzBdy0cVXZocN9tj7dpF8O83S1MH6Zu2GLrJ4hDzt4DHoPf2waGvbdPzaxu1-vL6w19hV601ic4P55n6Menj7erL8XN18_Xq4ubwjEppqKWjAE0ijipnSEgLBPOtLpVogVFjMu_VIK2UkFNqSKN0UbWptSKAtOl5Gfo3aFu7vDnDGmq-i4tY9kBwpwqThSTzOSd0bf_oHdhzqP4R0pyLmm5UPRAuRhSitBWY-x6G_cVJdViYnUwscomVouJ1UPWvDlWnusemj-KJ8sywA5AyqlhC_Hv0_-v-hutFqj7</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Hu, Zhijie</creator><creator>Li, Mengxia</creator><creator>Chen, Yufeng</creator><creator>Chen, Liutao</creator><creator>Han, Yuting</creator><creator>Chen, Chengyong</creator><creator>Lu, Xin</creator><creator>You, Nan</creator><creator>Lou, Yawen</creator><creator>Huang, Yingye</creator><creator>Huo, Zhanfeng</creator><creator>Liu, Chao</creator><creator>Liang, Cheng</creator><creator>Liu, Susu</creator><creator>Deng, Ke</creator><creator>Chen, Liangfu</creator><creator>Chen, Shangwu</creator><creator>Wan, Guohui</creator><creator>Wu, Xiaojian</creator><creator>Fu, Yonggui</creator><creator>Xu, Anlong</creator><general>Science China Press</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20240601</creationdate><title>Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1</title><author>Hu, Zhijie ; Li, Mengxia ; Chen, Yufeng ; Chen, Liutao ; Han, Yuting ; Chen, Chengyong ; Lu, Xin ; You, Nan ; Lou, Yawen ; Huang, Yingye ; Huo, Zhanfeng ; Liu, Chao ; Liang, Cheng ; Liu, Susu ; Deng, Ke ; Chen, Liangfu ; Chen, Shangwu ; Wan, Guohui ; Wu, Xiaojian ; Fu, Yonggui ; Xu, Anlong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c254t-b522eed60c57c80e4a24c8f7f64fe608c4959e7a56eb1160d8785b89761e27953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>3' Untranslated regions</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Life Sciences</topic><topic>Polyadenylation</topic><topic>Reseach Paper</topic><topic>Splicing factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Zhijie</creatorcontrib><creatorcontrib>Li, Mengxia</creatorcontrib><creatorcontrib>Chen, Yufeng</creatorcontrib><creatorcontrib>Chen, Liutao</creatorcontrib><creatorcontrib>Han, Yuting</creatorcontrib><creatorcontrib>Chen, Chengyong</creatorcontrib><creatorcontrib>Lu, Xin</creatorcontrib><creatorcontrib>You, Nan</creatorcontrib><creatorcontrib>Lou, Yawen</creatorcontrib><creatorcontrib>Huang, Yingye</creatorcontrib><creatorcontrib>Huo, Zhanfeng</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Liang, Cheng</creatorcontrib><creatorcontrib>Liu, Susu</creatorcontrib><creatorcontrib>Deng, Ke</creatorcontrib><creatorcontrib>Chen, Liangfu</creatorcontrib><creatorcontrib>Chen, Shangwu</creatorcontrib><creatorcontrib>Wan, Guohui</creatorcontrib><creatorcontrib>Wu, Xiaojian</creatorcontrib><creatorcontrib>Fu, Yonggui</creatorcontrib><creatorcontrib>Xu, Anlong</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Science China. Life sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Zhijie</au><au>Li, Mengxia</au><au>Chen, Yufeng</au><au>Chen, Liutao</au><au>Han, Yuting</au><au>Chen, Chengyong</au><au>Lu, Xin</au><au>You, Nan</au><au>Lou, Yawen</au><au>Huang, Yingye</au><au>Huo, Zhanfeng</au><au>Liu, Chao</au><au>Liang, Cheng</au><au>Liu, Susu</au><au>Deng, Ke</au><au>Chen, Liangfu</au><au>Chen, Shangwu</au><au>Wan, Guohui</au><au>Wu, Xiaojian</au><au>Fu, Yonggui</au><au>Xu, Anlong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1</atitle><jtitle>Science China. Life sciences</jtitle><stitle>Sci. China Life Sci</stitle><addtitle>Sci China Life Sci</addtitle><date>2024-06-01</date><risdate>2024</risdate><volume>67</volume><issue>6</issue><spage>1212</spage><epage>1225</epage><pages>1212-1225</pages><issn>1674-7305</issn><eissn>1869-1889</eissn><abstract>Generally shortened 3′ UTR due to alternative polyadenylation (APA) is widely observed in cancer, but its regulation mechanisms for cancer are not well characterized. Here, with profiling of APA in colorectal cancer tissues and poly(A) signal editing, we firstly identified that the shortened 3′ UTR of
CTNNIBP1
in colorectal cancer promotes cell proliferation and migration. We found that liquid-liquid phase separation (LLPS) of PABPN1 is reduced albeit with higher expression in cancer, and the reduction of LLPS leads to the shortened 3′ UTR of
CTNNBIP1
and promotes cell proliferation and migration. Notably, the splicing factor SNRPD2 upregulated in colorectal cancer, can interact with glutamic-proline (EP) domain of PABPN1, and then disrupt LLPS of PABPN1, which attenuates the repression effect of PABPN1 on the proximal poly(A) sites. Our results firstly reveal a new regulation mechanism of APA by disruption of LLPS of PABPN1, suggesting that regulation of APA by interfering LLPS of 3′ end processing factor may have the potential as a new way for the treatment of cancer.</abstract><cop>Beijing</cop><pub>Science China Press</pub><pmid>38811444</pmid><doi>10.1007/s11427-023-2495-x</doi><tpages>14</tpages></addata></record> |
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| source | SpringerLink Journals; Alma/SFX Local Collection |
| subjects | 3' Untranslated regions Biomedical and Life Sciences Cancer Cell growth Cell migration Cell proliferation Colorectal cancer Colorectal carcinoma Life Sciences Polyadenylation Reseach Paper Splicing factors |
| title | Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1 |
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