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BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1
Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcrip...
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| Published in: | Molecular carcinogenesis 2024-04, Vol.63 (4), p.663-676 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , |
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| container_end_page | 676 |
| container_issue | 4 |
| container_start_page | 663 |
| container_title | Molecular carcinogenesis |
| container_volume | 63 |
| creator | Li, Jiaying Yang, Ping Hong, Linjie Xiao, Wushuang Zhang, Luyu Yu, Zhen Zhang, Jieming Pei, Miaomiao Peng, Ying Wei, Xiangyang Wu, Xiaosheng Tang, Weimei Zhao, Yingying Yang, Juanying Lin, Zhizhao Jiang, Ping Xiang, Li Zhang, Hui Lin, Jianjiao Wang, Jide |
| description | Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcriptionally activated by homeobox D9 (HOXD9). BST2 was significantly upregulated in GC tissues and promoted epithelial–mesenchymal transition and metastasis of GC. BST2 knockdown reversed HOXD9's oncogenic effect on GC metastasis. Moreover, BST2 messenger RNA stability could be enhanced by poly(A) binding protein cytoplasmic 1 (PABPC1) through the interaction between BST2 3′‐UTR and PABPC1 in GC cells. PABPC1 promoted GC metastasis, which BST2 silencing attenuated in vitro and in vivo. In addition, positive correlations among HOXD9, BST2, and PABPC1 were established in clinical samples. Taken together, increased expression of BST2 induced by HOXD9 synergizing with PABPC1 promoted GC cell migration and invasion capacity. |
| doi_str_mv | 10.1002/mc.23679 |
| format | article |
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Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcriptionally activated by homeobox D9 (HOXD9). BST2 was significantly upregulated in GC tissues and promoted epithelial–mesenchymal transition and metastasis of GC. BST2 knockdown reversed HOXD9's oncogenic effect on GC metastasis. Moreover, BST2 messenger RNA stability could be enhanced by poly(A) binding protein cytoplasmic 1 (PABPC1) through the interaction between BST2 3′‐UTR and PABPC1 in GC cells. PABPC1 promoted GC metastasis, which BST2 silencing attenuated in vitro and in vivo. In addition, positive correlations among HOXD9, BST2, and PABPC1 were established in clinical samples. Taken together, increased expression of BST2 induced by HOXD9 synergizing with PABPC1 promoted GC cell migration and invasion capacity.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.23679</identifier><identifier>PMID: 38197534</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>3' Untranslated regions ; Bone cancer ; BST2 ; Cell migration ; Gastric cancer ; Homeobox ; HOXD9 ; Metastases ; Metastasis ; Mortality ; mRNA stability ; PABPC1</subject><ispartof>Molecular carcinogenesis, 2024-04, Vol.63 (4), p.663-676</ispartof><rights>2024 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3109-ffd567714eab03818e68c43096ff17c6226b91dddf74e7ed22bbba5d0e9986793</cites><orcidid>0000-0001-7508-1579 ; 0000-0002-0988-9454</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38197534$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jiaying</creatorcontrib><creatorcontrib>Yang, Ping</creatorcontrib><creatorcontrib>Hong, Linjie</creatorcontrib><creatorcontrib>Xiao, Wushuang</creatorcontrib><creatorcontrib>Zhang, Luyu</creatorcontrib><creatorcontrib>Yu, Zhen</creatorcontrib><creatorcontrib>Zhang, Jieming</creatorcontrib><creatorcontrib>Pei, Miaomiao</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><creatorcontrib>Wei, Xiangyang</creatorcontrib><creatorcontrib>Wu, Xiaosheng</creatorcontrib><creatorcontrib>Tang, Weimei</creatorcontrib><creatorcontrib>Zhao, Yingying</creatorcontrib><creatorcontrib>Yang, Juanying</creatorcontrib><creatorcontrib>Lin, Zhizhao</creatorcontrib><creatorcontrib>Jiang, Ping</creatorcontrib><creatorcontrib>Xiang, Li</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Lin, Jianjiao</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><title>BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1</title><title>Molecular carcinogenesis</title><addtitle>Mol Carcinog</addtitle><description>Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcriptionally activated by homeobox D9 (HOXD9). BST2 was significantly upregulated in GC tissues and promoted epithelial–mesenchymal transition and metastasis of GC. BST2 knockdown reversed HOXD9's oncogenic effect on GC metastasis. Moreover, BST2 messenger RNA stability could be enhanced by poly(A) binding protein cytoplasmic 1 (PABPC1) through the interaction between BST2 3′‐UTR and PABPC1 in GC cells. PABPC1 promoted GC metastasis, which BST2 silencing attenuated in vitro and in vivo. In addition, positive correlations among HOXD9, BST2, and PABPC1 were established in clinical samples. Taken together, increased expression of BST2 induced by HOXD9 synergizing with PABPC1 promoted GC cell migration and invasion capacity.</description><subject>3' Untranslated regions</subject><subject>Bone cancer</subject><subject>BST2</subject><subject>Cell migration</subject><subject>Gastric cancer</subject><subject>Homeobox</subject><subject>HOXD9</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mortality</subject><subject>mRNA stability</subject><subject>PABPC1</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp1kF1LwzAUhoMobk7BXyABb7zpTNI2aS63-TFhsoETvCtpcjo7-jGTFtm_N7qpIHh14OXh4T0vQueUDCkh7LrSQxZyIQ9QnxKZBExE0SHqk0TKgMpE9NCJc2tCKBUxOUa9MKFSxGHUR4vx05LhjW2qpgWHV8q1ttBYq1qDxRW0PlCucLirjQ_aV8AWVl2p2qKpcZPj6fzlRmJVG7wYjRcTeoqOclU6ONvfAXq-u11OpsFsfv8wGc0CHfqKQZ6bmAtBI1AZ8XUS4ImOQiJ5nlOhOWM8k9QYk4sIBBjGsixTsSEgZeI_DQfoauf13d86cG1aFU5DWaoams6lTNKQeG8Ue_TyD7puOlv7dp6KOeeMROxXqG3jnIU83diiUnabUpJ-rpxWOv1a2aMXe2GXVWB-wO9ZPRDsgPeihO2_ovRxshN-AEjxgqo</recordid><startdate>202404</startdate><enddate>202404</enddate><creator>Li, Jiaying</creator><creator>Yang, Ping</creator><creator>Hong, Linjie</creator><creator>Xiao, Wushuang</creator><creator>Zhang, Luyu</creator><creator>Yu, Zhen</creator><creator>Zhang, Jieming</creator><creator>Pei, Miaomiao</creator><creator>Peng, Ying</creator><creator>Wei, Xiangyang</creator><creator>Wu, Xiaosheng</creator><creator>Tang, Weimei</creator><creator>Zhao, Yingying</creator><creator>Yang, Juanying</creator><creator>Lin, Zhizhao</creator><creator>Jiang, Ping</creator><creator>Xiang, Li</creator><creator>Zhang, Hui</creator><creator>Lin, Jianjiao</creator><creator>Wang, Jide</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7508-1579</orcidid><orcidid>https://orcid.org/0000-0002-0988-9454</orcidid></search><sort><creationdate>202404</creationdate><title>BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1</title><author>Li, Jiaying ; Yang, Ping ; Hong, Linjie ; Xiao, Wushuang ; Zhang, Luyu ; Yu, Zhen ; Zhang, Jieming ; Pei, Miaomiao ; Peng, Ying ; Wei, Xiangyang ; Wu, Xiaosheng ; Tang, Weimei ; Zhao, Yingying ; Yang, Juanying ; Lin, Zhizhao ; Jiang, Ping ; Xiang, Li ; Zhang, Hui ; Lin, Jianjiao ; Wang, Jide</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3109-ffd567714eab03818e68c43096ff17c6226b91dddf74e7ed22bbba5d0e9986793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>3' Untranslated regions</topic><topic>Bone cancer</topic><topic>BST2</topic><topic>Cell migration</topic><topic>Gastric cancer</topic><topic>Homeobox</topic><topic>HOXD9</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mortality</topic><topic>mRNA stability</topic><topic>PABPC1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jiaying</creatorcontrib><creatorcontrib>Yang, Ping</creatorcontrib><creatorcontrib>Hong, Linjie</creatorcontrib><creatorcontrib>Xiao, Wushuang</creatorcontrib><creatorcontrib>Zhang, Luyu</creatorcontrib><creatorcontrib>Yu, Zhen</creatorcontrib><creatorcontrib>Zhang, Jieming</creatorcontrib><creatorcontrib>Pei, Miaomiao</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><creatorcontrib>Wei, Xiangyang</creatorcontrib><creatorcontrib>Wu, Xiaosheng</creatorcontrib><creatorcontrib>Tang, Weimei</creatorcontrib><creatorcontrib>Zhao, Yingying</creatorcontrib><creatorcontrib>Yang, Juanying</creatorcontrib><creatorcontrib>Lin, Zhizhao</creatorcontrib><creatorcontrib>Jiang, Ping</creatorcontrib><creatorcontrib>Xiang, Li</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Lin, Jianjiao</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jiaying</au><au>Yang, Ping</au><au>Hong, Linjie</au><au>Xiao, Wushuang</au><au>Zhang, Luyu</au><au>Yu, Zhen</au><au>Zhang, Jieming</au><au>Pei, Miaomiao</au><au>Peng, Ying</au><au>Wei, Xiangyang</au><au>Wu, Xiaosheng</au><au>Tang, Weimei</au><au>Zhao, Yingying</au><au>Yang, Juanying</au><au>Lin, Zhizhao</au><au>Jiang, Ping</au><au>Xiang, Li</au><au>Zhang, Hui</au><au>Lin, Jianjiao</au><au>Wang, Jide</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol Carcinog</addtitle><date>2024-04</date><risdate>2024</risdate><volume>63</volume><issue>4</issue><spage>663</spage><epage>676</epage><pages>663-676</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>Gastric cancer (GC) constitutes substantial cancer mortality worldwide. Several cancer types aberrantly express bone marrow stromal cell antigen 2 (BST2), yet its functional and underlying mechanisms in GC progression remain unknown. In our study, RNA sequencing data revealed that BST2 was transcriptionally activated by homeobox D9 (HOXD9). BST2 was significantly upregulated in GC tissues and promoted epithelial–mesenchymal transition and metastasis of GC. BST2 knockdown reversed HOXD9's oncogenic effect on GC metastasis. Moreover, BST2 messenger RNA stability could be enhanced by poly(A) binding protein cytoplasmic 1 (PABPC1) through the interaction between BST2 3′‐UTR and PABPC1 in GC cells. PABPC1 promoted GC metastasis, which BST2 silencing attenuated in vitro and in vivo. In addition, positive correlations among HOXD9, BST2, and PABPC1 were established in clinical samples. Taken together, increased expression of BST2 induced by HOXD9 synergizing with PABPC1 promoted GC cell migration and invasion capacity.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>38197534</pmid><doi>10.1002/mc.23679</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7508-1579</orcidid><orcidid>https://orcid.org/0000-0002-0988-9454</orcidid></addata></record> |
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| identifier | ISSN: 0899-1987 |
| ispartof | Molecular carcinogenesis, 2024-04, Vol.63 (4), p.663-676 |
| issn | 0899-1987 1098-2744 |
| language | eng |
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| source | Wiley-Blackwell Read & Publish Collection |
| subjects | 3' Untranslated regions Bone cancer BST2 Cell migration Gastric cancer Homeobox HOXD9 Metastases Metastasis Mortality mRNA stability PABPC1 |
| title | BST2 promotes gastric cancer metastasis under the regulation of HOXD9 and PABPC1 |
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