NAT10 functions as a pivotal regulator in gastric cancer metastasis and tumor immunity
Gastric cancer (GC) presents a significant global health burden, with metastasis being the leading cause of treatment failure and mortality. NAT10, a regulatory protein involved in mRNA acetylation, has been implicated in various cancers. However, its role in GC, especially concerning metastasis and...
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Veröffentlicht in: | Journal of cellular physiology 2025-01, Vol.240 (1), p.e31474 |
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container_title | Journal of cellular physiology |
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creator | Mo, Yuqian Huang, Enyu Deng, Chao Huang, Haofeng Zhu, Ying Wei, Xinlong Zhong, Jinlin Wang, Yuzhi Huang, Zhigang Zhang, Jingjing |
description | Gastric cancer (GC) presents a significant global health burden, with metastasis being the leading cause of treatment failure and mortality. NAT10, a regulatory protein involved in mRNA acetylation, has been implicated in various cancers. However, its role in GC, especially concerning metastasis and immune interactions, remains unclear. Utilizing multi-omics data from gastric cancer samples, we conducted comprehensive analyses to investigate NAT10 expression, its correlation with clinical parameters and immune relevance. Bioinformatics analysis and digital image processing were employed for this purpose. Furthermore, in vitro and in vivo experiments were conducted to elucidate the functional role of NAT10 in gastric cancer progression, aiming to provide deeper biological insights. Our findings reveal a significant association between NAT10 expression and various aspects of transcriptional, protein, as well as tumor immunity in GC patients. Additionally, we demonstrated that NAT10 promotes gastric cancer cell proliferation and migration, both in cellular models and in animal studies, suggesting its involvement in early tumor microvascular metastasis. NAT10 emerges as a promising molecular target, offering potential avenues for further research into molecular mechanisms and therapeutic strategies for GC. |
doi_str_mv | 10.1002/jcp.31474 |
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NAT10, a regulatory protein involved in mRNA acetylation, has been implicated in various cancers. However, its role in GC, especially concerning metastasis and immune interactions, remains unclear. Utilizing multi-omics data from gastric cancer samples, we conducted comprehensive analyses to investigate NAT10 expression, its correlation with clinical parameters and immune relevance. Bioinformatics analysis and digital image processing were employed for this purpose. Furthermore, in vitro and in vivo experiments were conducted to elucidate the functional role of NAT10 in gastric cancer progression, aiming to provide deeper biological insights. Our findings reveal a significant association between NAT10 expression and various aspects of transcriptional, protein, as well as tumor immunity in GC patients. Additionally, we demonstrated that NAT10 promotes gastric cancer cell proliferation and migration, both in cellular models and in animal studies, suggesting its involvement in early tumor microvascular metastasis. NAT10 emerges as a promising molecular target, offering potential avenues for further research into molecular mechanisms and therapeutic strategies for GC.</description><identifier>ISSN: 0021-9541</identifier><identifier>ISSN: 1097-4652</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.31474</identifier><identifier>PMID: 39467076</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; N-Terminal Acetyltransferase E - genetics ; N-Terminal Acetyltransferase E - metabolism ; Neoplasm Metastasis ; Stomach Neoplasms - genetics ; Stomach Neoplasms - immunology ; Stomach Neoplasms - pathology</subject><ispartof>Journal of cellular physiology, 2025-01, Vol.240 (1), p.e31474</ispartof><rights>2024 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c175t-2d0c48847de2c351d74e7d0f823ef7f9c38a994c008a46d6eb70baa646eef70c3</cites><orcidid>0000-0002-8789-4638</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39467076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mo, Yuqian</creatorcontrib><creatorcontrib>Huang, Enyu</creatorcontrib><creatorcontrib>Deng, Chao</creatorcontrib><creatorcontrib>Huang, Haofeng</creatorcontrib><creatorcontrib>Zhu, Ying</creatorcontrib><creatorcontrib>Wei, Xinlong</creatorcontrib><creatorcontrib>Zhong, Jinlin</creatorcontrib><creatorcontrib>Wang, Yuzhi</creatorcontrib><creatorcontrib>Huang, Zhigang</creatorcontrib><creatorcontrib>Zhang, Jingjing</creatorcontrib><title>NAT10 functions as a pivotal regulator in gastric cancer metastasis and tumor immunity</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Gastric cancer (GC) presents a significant global health burden, with metastasis being the leading cause of treatment failure and mortality. NAT10, a regulatory protein involved in mRNA acetylation, has been implicated in various cancers. However, its role in GC, especially concerning metastasis and immune interactions, remains unclear. Utilizing multi-omics data from gastric cancer samples, we conducted comprehensive analyses to investigate NAT10 expression, its correlation with clinical parameters and immune relevance. Bioinformatics analysis and digital image processing were employed for this purpose. Furthermore, in vitro and in vivo experiments were conducted to elucidate the functional role of NAT10 in gastric cancer progression, aiming to provide deeper biological insights. Our findings reveal a significant association between NAT10 expression and various aspects of transcriptional, protein, as well as tumor immunity in GC patients. Additionally, we demonstrated that NAT10 promotes gastric cancer cell proliferation and migration, both in cellular models and in animal studies, suggesting its involvement in early tumor microvascular metastasis. NAT10 emerges as a promising molecular target, offering potential avenues for further research into molecular mechanisms and therapeutic strategies for GC.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>N-Terminal Acetyltransferase E - genetics</subject><subject>N-Terminal Acetyltransferase E - metabolism</subject><subject>Neoplasm Metastasis</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - immunology</subject><subject>Stomach Neoplasms - pathology</subject><issn>0021-9541</issn><issn>1097-4652</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LAzEQhoMotlYP_gHJUQ9bJ5tssjmW4hcUvVSvIc1mS8p-mWSF_ntTq8LAwLzPDMyD0DWBOQHI73dmmFPCBDtBUwJSZIwX-SmapoxksmBkgi5C2AGAlJSeowmVjAsQfIo-XhdrArgeOxNd3wWsU-HBffVRN9jb7djo2HvsOrzVIXpnsNGdsR63NqaBDi4tdBWOY3vA2nbsXNxforNaN8Fe_fYZen98WC-fs9Xb08tyscoMEUXM8goMK0smKpsbWpBKMCsqqMuc2lrU0tBSS8kMQKkZr7jdCNhozRm3KQdDZ-j2eHfw_edoQ1StC8Y2je5sPwZFSU6KUhbp7Rm6O6LG9yF4W6vBu1b7vSKgDhpV0qh-NCb25vfsuGlt9U_-eaPf6cJt6g</recordid><startdate>202501</startdate><enddate>202501</enddate><creator>Mo, Yuqian</creator><creator>Huang, Enyu</creator><creator>Deng, Chao</creator><creator>Huang, Haofeng</creator><creator>Zhu, Ying</creator><creator>Wei, Xinlong</creator><creator>Zhong, Jinlin</creator><creator>Wang, Yuzhi</creator><creator>Huang, Zhigang</creator><creator>Zhang, Jingjing</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8789-4638</orcidid></search><sort><creationdate>202501</creationdate><title>NAT10 functions as a pivotal regulator in gastric cancer metastasis and tumor immunity</title><author>Mo, Yuqian ; Huang, Enyu ; Deng, Chao ; Huang, Haofeng ; Zhu, Ying ; Wei, Xinlong ; Zhong, Jinlin ; Wang, Yuzhi ; Huang, Zhigang ; Zhang, Jingjing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c175t-2d0c48847de2c351d74e7d0f823ef7f9c38a994c008a46d6eb70baa646eef70c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>N-Terminal Acetyltransferase E - genetics</topic><topic>N-Terminal Acetyltransferase E - metabolism</topic><topic>Neoplasm Metastasis</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - immunology</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mo, Yuqian</creatorcontrib><creatorcontrib>Huang, Enyu</creatorcontrib><creatorcontrib>Deng, Chao</creatorcontrib><creatorcontrib>Huang, Haofeng</creatorcontrib><creatorcontrib>Zhu, Ying</creatorcontrib><creatorcontrib>Wei, Xinlong</creatorcontrib><creatorcontrib>Zhong, Jinlin</creatorcontrib><creatorcontrib>Wang, Yuzhi</creatorcontrib><creatorcontrib>Huang, Zhigang</creatorcontrib><creatorcontrib>Zhang, Jingjing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mo, Yuqian</au><au>Huang, Enyu</au><au>Deng, Chao</au><au>Huang, Haofeng</au><au>Zhu, Ying</au><au>Wei, Xinlong</au><au>Zhong, Jinlin</au><au>Wang, Yuzhi</au><au>Huang, Zhigang</au><au>Zhang, Jingjing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NAT10 functions as a pivotal regulator in gastric cancer metastasis and tumor immunity</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2025-01</date><risdate>2025</risdate><volume>240</volume><issue>1</issue><spage>e31474</spage><pages>e31474-</pages><issn>0021-9541</issn><issn>1097-4652</issn><eissn>1097-4652</eissn><abstract>Gastric cancer (GC) presents a significant global health burden, with metastasis being the leading cause of treatment failure and mortality. NAT10, a regulatory protein involved in mRNA acetylation, has been implicated in various cancers. However, its role in GC, especially concerning metastasis and immune interactions, remains unclear. Utilizing multi-omics data from gastric cancer samples, we conducted comprehensive analyses to investigate NAT10 expression, its correlation with clinical parameters and immune relevance. Bioinformatics analysis and digital image processing were employed for this purpose. Furthermore, in vitro and in vivo experiments were conducted to elucidate the functional role of NAT10 in gastric cancer progression, aiming to provide deeper biological insights. Our findings reveal a significant association between NAT10 expression and various aspects of transcriptional, protein, as well as tumor immunity in GC patients. Additionally, we demonstrated that NAT10 promotes gastric cancer cell proliferation and migration, both in cellular models and in animal studies, suggesting its involvement in early tumor microvascular metastasis. NAT10 emerges as a promising molecular target, offering potential avenues for further research into molecular mechanisms and therapeutic strategies for GC.</abstract><cop>United States</cop><pmid>39467076</pmid><doi>10.1002/jcp.31474</doi><orcidid>https://orcid.org/0000-0002-8789-4638</orcidid></addata></record> |
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subjects | Animals Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Female Gene Expression Regulation, Neoplastic - genetics Humans Male Mice Mice, Inbred BALB C Mice, Nude N-Terminal Acetyltransferase E - genetics N-Terminal Acetyltransferase E - metabolism Neoplasm Metastasis Stomach Neoplasms - genetics Stomach Neoplasms - immunology Stomach Neoplasms - pathology |
title | NAT10 functions as a pivotal regulator in gastric cancer metastasis and tumor immunity |
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