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Deletion of TMEM268 inhibits growth of gastric cancer cells by downregulating the ITGB4 signaling pathway
Transmembrane protein 268 ( TMEM268 ) encodes a novel human protein of previously unknown function. This study analyzed the biological activities and molecular mechanisms of TMEM268 in vivo and in vitro. We found that TMEM268 deletion decreases cell viability, proliferation, and cell adhesion as wel...
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| Published in: | Cell death and differentiation 2019-08, Vol.26 (8), p.1453-1466 |
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| container_end_page | 1466 |
| container_issue | 8 |
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| container_title | Cell death and differentiation |
| container_volume | 26 |
| creator | Hong, Dubeiqi Zhang, Xuan Li, Riyong Yu, Jiahong Lou, Yaxin He, Qihua Li, Xuanze Xu, Dong Lv, Ping Lin, Jian Chen, Yingyu |
| description | Transmembrane protein 268 (
TMEM268
) encodes a novel human protein of previously unknown function. This study analyzed the biological activities and molecular mechanisms of TMEM268 in vivo and in vitro. We found that
TMEM268
deletion decreases cell viability, proliferation, and cell adhesion as well as causing S-phase cell cycle arrest and disrupts cytoskeleton remolding. Xenograft tumor mouse model studies showed that
TMEM268
deletion inhibits the tumorigenesis of BGC823 gastric cancer cells. In addition,
TMEM268-
deleted BGC823 cells failed to colonize the lungs after intravenous injection and to form metastatic engraftment in the peritoneum. Molecular mechanism studies showed a C-terminal interaction between TMEM268 and integrin subunit β4 (ITGB4).
TMEM268
knockout promotes ITGB4 ubiquitin-mediated degradation, increasing the instability of ITGB4 and filamin A (FLNA). The reduced ITGB4 protein levels result in the disassociation of the ITGB4/PLEC complex and cytoskeleton remodeling. This study for the first time demonstrates that TMEM268 plays a positive role in the regulation of ITGB4 homeostasis. The above results may provide a new perspective that targeting the TMEM268/ITGB4 signaling axis for the treatment of gastric cancer, which deserves further investigation in the future. |
| doi_str_mv | 10.1038/s41418-018-0223-3 |
| format | article |
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TMEM268
) encodes a novel human protein of previously unknown function. This study analyzed the biological activities and molecular mechanisms of TMEM268 in vivo and in vitro. We found that
TMEM268
deletion decreases cell viability, proliferation, and cell adhesion as well as causing S-phase cell cycle arrest and disrupts cytoskeleton remolding. Xenograft tumor mouse model studies showed that
TMEM268
deletion inhibits the tumorigenesis of BGC823 gastric cancer cells. In addition,
TMEM268-
deleted BGC823 cells failed to colonize the lungs after intravenous injection and to form metastatic engraftment in the peritoneum. Molecular mechanism studies showed a C-terminal interaction between TMEM268 and integrin subunit β4 (ITGB4).
TMEM268
knockout promotes ITGB4 ubiquitin-mediated degradation, increasing the instability of ITGB4 and filamin A (FLNA). The reduced ITGB4 protein levels result in the disassociation of the ITGB4/PLEC complex and cytoskeleton remodeling. This study for the first time demonstrates that TMEM268 plays a positive role in the regulation of ITGB4 homeostasis. The above results may provide a new perspective that targeting the TMEM268/ITGB4 signaling axis for the treatment of gastric cancer, which deserves further investigation in the future.</description><identifier>ISSN: 1350-9047</identifier><identifier>EISSN: 1476-5403</identifier><identifier>DOI: 10.1038/s41418-018-0223-3</identifier><identifier>PMID: 30361615</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/2 ; 13/51 ; 14 ; 14/1 ; 14/19 ; 14/28 ; 14/34 ; 38 ; 631/67/1244 ; 631/80/79/1236 ; 82/80 ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Cell adhesion ; Cell adhesion & migration ; Cell Biology ; Cell cycle ; Cell Cycle Analysis ; Cell viability ; Clonal deletion ; Cytoskeleton ; Gastric cancer ; Homeostasis ; Intravenous administration ; Life Sciences ; Metastases ; Molecular modelling ; Peritoneum ; Proteins ; Signal transduction ; Stem Cells ; Tumorigenesis ; Ubiquitin ; Xenografts</subject><ispartof>Cell death and differentiation, 2019-08, Vol.26 (8), p.1453-1466</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-45681c2d92f9907c730d755a908f41a0e7e139feefdad72a855c3c753988e223</citedby><cites>FETCH-LOGICAL-c470t-45681c2d92f9907c730d755a908f41a0e7e139feefdad72a855c3c753988e223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748091/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748091/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30361615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hong, Dubeiqi</creatorcontrib><creatorcontrib>Zhang, Xuan</creatorcontrib><creatorcontrib>Li, Riyong</creatorcontrib><creatorcontrib>Yu, Jiahong</creatorcontrib><creatorcontrib>Lou, Yaxin</creatorcontrib><creatorcontrib>He, Qihua</creatorcontrib><creatorcontrib>Li, Xuanze</creatorcontrib><creatorcontrib>Xu, Dong</creatorcontrib><creatorcontrib>Lv, Ping</creatorcontrib><creatorcontrib>Lin, Jian</creatorcontrib><creatorcontrib>Chen, Yingyu</creatorcontrib><title>Deletion of TMEM268 inhibits growth of gastric cancer cells by downregulating the ITGB4 signaling pathway</title><title>Cell death and differentiation</title><addtitle>Cell Death Differ</addtitle><addtitle>Cell Death Differ</addtitle><description>Transmembrane protein 268 (
TMEM268
) encodes a novel human protein of previously unknown function. This study analyzed the biological activities and molecular mechanisms of TMEM268 in vivo and in vitro. We found that
TMEM268
deletion decreases cell viability, proliferation, and cell adhesion as well as causing S-phase cell cycle arrest and disrupts cytoskeleton remolding. Xenograft tumor mouse model studies showed that
TMEM268
deletion inhibits the tumorigenesis of BGC823 gastric cancer cells. In addition,
TMEM268-
deleted BGC823 cells failed to colonize the lungs after intravenous injection and to form metastatic engraftment in the peritoneum. Molecular mechanism studies showed a C-terminal interaction between TMEM268 and integrin subunit β4 (ITGB4).
TMEM268
knockout promotes ITGB4 ubiquitin-mediated degradation, increasing the instability of ITGB4 and filamin A (FLNA). The reduced ITGB4 protein levels result in the disassociation of the ITGB4/PLEC complex and cytoskeleton remodeling. This study for the first time demonstrates that TMEM268 plays a positive role in the regulation of ITGB4 homeostasis. The above results may provide a new perspective that targeting the TMEM268/ITGB4 signaling axis for the treatment of gastric cancer, which deserves further investigation in the future.</description><subject>13</subject><subject>13/2</subject><subject>13/51</subject><subject>14</subject><subject>14/1</subject><subject>14/19</subject><subject>14/28</subject><subject>14/34</subject><subject>38</subject><subject>631/67/1244</subject><subject>631/80/79/1236</subject><subject>82/80</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle Analysis</subject><subject>Cell viability</subject><subject>Clonal deletion</subject><subject>Cytoskeleton</subject><subject>Gastric cancer</subject><subject>Homeostasis</subject><subject>Intravenous administration</subject><subject>Life 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inhibits growth of gastric cancer cells by downregulating the ITGB4 signaling pathway</title><author>Hong, Dubeiqi ; Zhang, Xuan ; Li, Riyong ; Yu, Jiahong ; Lou, Yaxin ; He, Qihua ; Li, Xuanze ; Xu, Dong ; Lv, Ping ; Lin, Jian ; Chen, Yingyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-45681c2d92f9907c730d755a908f41a0e7e139feefdad72a855c3c753988e223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13</topic><topic>13/2</topic><topic>13/51</topic><topic>14</topic><topic>14/1</topic><topic>14/19</topic><topic>14/28</topic><topic>14/34</topic><topic>38</topic><topic>631/67/1244</topic><topic>631/80/79/1236</topic><topic>82/80</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Cycle 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Yingyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deletion of TMEM268 inhibits growth of gastric cancer cells by downregulating the ITGB4 signaling pathway</atitle><jtitle>Cell death and differentiation</jtitle><stitle>Cell Death Differ</stitle><addtitle>Cell Death Differ</addtitle><date>2019-08-01</date><risdate>2019</risdate><volume>26</volume><issue>8</issue><spage>1453</spage><epage>1466</epage><pages>1453-1466</pages><issn>1350-9047</issn><eissn>1476-5403</eissn><abstract>Transmembrane protein 268 (
TMEM268
) encodes a novel human protein of previously unknown function. This study analyzed the biological activities and molecular mechanisms of TMEM268 in vivo and in vitro. We found that
TMEM268
deletion decreases cell viability, proliferation, and cell adhesion as well as causing S-phase cell cycle arrest and disrupts cytoskeleton remolding. Xenograft tumor mouse model studies showed that
TMEM268
deletion inhibits the tumorigenesis of BGC823 gastric cancer cells. In addition,
TMEM268-
deleted BGC823 cells failed to colonize the lungs after intravenous injection and to form metastatic engraftment in the peritoneum. Molecular mechanism studies showed a C-terminal interaction between TMEM268 and integrin subunit β4 (ITGB4).
TMEM268
knockout promotes ITGB4 ubiquitin-mediated degradation, increasing the instability of ITGB4 and filamin A (FLNA). The reduced ITGB4 protein levels result in the disassociation of the ITGB4/PLEC complex and cytoskeleton remodeling. This study for the first time demonstrates that TMEM268 plays a positive role in the regulation of ITGB4 homeostasis. The above results may provide a new perspective that targeting the TMEM268/ITGB4 signaling axis for the treatment of gastric cancer, which deserves further investigation in the future.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30361615</pmid><doi>10.1038/s41418-018-0223-3</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death and differentiation, 2019-08, Vol.26 (8), p.1453-1466 |
| issn | 1350-9047 1476-5403 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6748091 |
| source | Open Access: PubMed Central; Springer Link |
| subjects | 13 13/2 13/51 14 14/1 14/19 14/28 14/34 38 631/67/1244 631/80/79/1236 82/80 Apoptosis Biochemistry Biomedical and Life Sciences Cell adhesion Cell adhesion & migration Cell Biology Cell cycle Cell Cycle Analysis Cell viability Clonal deletion Cytoskeleton Gastric cancer Homeostasis Intravenous administration Life Sciences Metastases Molecular modelling Peritoneum Proteins Signal transduction Stem Cells Tumorigenesis Ubiquitin Xenografts |
| title | Deletion of TMEM268 inhibits growth of gastric cancer cells by downregulating the ITGB4 signaling pathway |
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