N-3, a novel synthetic derivative of bifendate, inhibits metastasis of triple-negative breast cancer via decreasing p38-regulated FOXC1 protein stability
[Display omitted] Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high invasiveness, metastatic potential, and poor prognosis. Epithelial–mesenchymal transition (EMT) is pivotal in TNBC progression, becoming a promising target for TNBC treatment. Our study evaluated...
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| Veröffentlicht in: | Biochemical pharmacology 2023-09, Vol.215, p.115729-115729, Article 115729 |
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| container_title | Biochemical pharmacology |
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| creator | Wang, Fan Liao, Rong Wang, Xin Xiong, Guixiang Zhang, Beibei Li, Juan Wu, Dengpan Chen, Yan Zhou, Xueyan Gu, Xiaoke Qi, Qi Li, Chenglin |
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Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high invasiveness, metastatic potential, and poor prognosis. Epithelial–mesenchymal transition (EMT) is pivotal in TNBC progression, becoming a promising target for TNBC treatment. Our study evaluated N-3, a novel synthetic bifendate derivative, which inhibited the EMT-associated migration and invasion of MDA-MB-231 and 4T1 TNBC cells. The results were consistent with the suppression of FOXC1 expression and transcriptional activity. Additional studies indicated that N-3 reduced the protein stability of FOXC1 by enhancing ubiquitination and degradation. Moreover, N-3 downregulated p-p38 expression and FOXC1 interaction, decreasing the stability of p38-regulated FOXC1. Further, N-3 blocked TNBC metastasis with an artificial lung metastasis model in vivo, related to FOXC1 suppression and EMT. These results highlight the potential of N-3 as a TNBC metastasis treatment. Therefore, FOXC1 regulation could be a novel targeted therapeutic strategy for TNBC metastasis. |
| doi_str_mv | 10.1016/j.bcp.2023.115729 |
| format | Article |
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Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high invasiveness, metastatic potential, and poor prognosis. Epithelial–mesenchymal transition (EMT) is pivotal in TNBC progression, becoming a promising target for TNBC treatment. Our study evaluated N-3, a novel synthetic bifendate derivative, which inhibited the EMT-associated migration and invasion of MDA-MB-231 and 4T1 TNBC cells. The results were consistent with the suppression of FOXC1 expression and transcriptional activity. Additional studies indicated that N-3 reduced the protein stability of FOXC1 by enhancing ubiquitination and degradation. Moreover, N-3 downregulated p-p38 expression and FOXC1 interaction, decreasing the stability of p38-regulated FOXC1. Further, N-3 blocked TNBC metastasis with an artificial lung metastasis model in vivo, related to FOXC1 suppression and EMT. These results highlight the potential of N-3 as a TNBC metastasis treatment. Therefore, FOXC1 regulation could be a novel targeted therapeutic strategy for TNBC metastasis.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2023.115729</identifier><identifier>PMID: 37558004</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Epithelial–mesenchymal transition ; FOXC1 stability ; Metastasis ; N-3 ; P38 ; Triple-negative breast cancer</subject><ispartof>Biochemical pharmacology, 2023-09, Vol.215, p.115729-115729, Article 115729</ispartof><rights>2023 Elsevier Inc.</rights><rights>Copyright © 2023. Published by Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c353t-875f5b42f34b38824b5dd1a9d06428da8948ae8fcf8bea3511bfb8987067dc373</citedby><cites>FETCH-LOGICAL-c353t-875f5b42f34b38824b5dd1a9d06428da8948ae8fcf8bea3511bfb8987067dc373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bcp.2023.115729$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37558004$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Fan</creatorcontrib><creatorcontrib>Liao, Rong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Xiong, Guixiang</creatorcontrib><creatorcontrib>Zhang, Beibei</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><creatorcontrib>Wu, Dengpan</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Zhou, Xueyan</creatorcontrib><creatorcontrib>Gu, Xiaoke</creatorcontrib><creatorcontrib>Qi, Qi</creatorcontrib><creatorcontrib>Li, Chenglin</creatorcontrib><title>N-3, a novel synthetic derivative of bifendate, inhibits metastasis of triple-negative breast cancer via decreasing p38-regulated FOXC1 protein stability</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>[Display omitted]
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high invasiveness, metastatic potential, and poor prognosis. Epithelial–mesenchymal transition (EMT) is pivotal in TNBC progression, becoming a promising target for TNBC treatment. Our study evaluated N-3, a novel synthetic bifendate derivative, which inhibited the EMT-associated migration and invasion of MDA-MB-231 and 4T1 TNBC cells. The results were consistent with the suppression of FOXC1 expression and transcriptional activity. Additional studies indicated that N-3 reduced the protein stability of FOXC1 by enhancing ubiquitination and degradation. Moreover, N-3 downregulated p-p38 expression and FOXC1 interaction, decreasing the stability of p38-regulated FOXC1. Further, N-3 blocked TNBC metastasis with an artificial lung metastasis model in vivo, related to FOXC1 suppression and EMT. These results highlight the potential of N-3 as a TNBC metastasis treatment. Therefore, FOXC1 regulation could be a novel targeted therapeutic strategy for TNBC metastasis.</description><subject>Epithelial–mesenchymal transition</subject><subject>FOXC1 stability</subject><subject>Metastasis</subject><subject>N-3</subject><subject>P38</subject><subject>Triple-negative breast cancer</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kc2KFDEUhYMoTjv6AG4kSxdTbVKpn1u4ksZRYXA2Cu5Cfm713Ka6qk3SBf0o87amqNGlEEhu7jkfyT2MvZViK4VsPhy21p22pSjVVsq6LbtnbCOhVUXZNfCcbYQQTT7X5RV7FeNhKaGRL9mVausahKg27PF7oW644eM048DjZUwPmMhxj4Fmk2hGPvXcUo-jNwlvOI0PZClFfsRkYl4UF0UKdBqwGHG_mmzA3OXOjA4Dn8lkolvuaNzzk4Ii4P48ZKLnt_e_dpKfwpSQRp6RlgZKl9fsRW-GiG-e9mv28_bzj93X4u7-y7fdp7vCqVqlAtq6r21V9qqyCqCsbO29NJ0XTVWCN9BVYBB614NFo2opbW-hg1Y0rXeqVdfs_crNL_h9xpj0kaLDYTAjTueoS6gAqqqDLkvlKnVhijFgr0-BjiZctBR6SUQfdE5EL4noNZHsefeEP9sj-n-OvxFkwcdVgPmTM2HQ0RHmsXkK6JL2E_0H_wdQBJ2k</recordid><startdate>20230901</startdate><enddate>20230901</enddate><creator>Wang, Fan</creator><creator>Liao, Rong</creator><creator>Wang, Xin</creator><creator>Xiong, Guixiang</creator><creator>Zhang, Beibei</creator><creator>Li, Juan</creator><creator>Wu, Dengpan</creator><creator>Chen, Yan</creator><creator>Zhou, Xueyan</creator><creator>Gu, Xiaoke</creator><creator>Qi, Qi</creator><creator>Li, Chenglin</creator><general>Elsevier Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20230901</creationdate><title>N-3, a novel synthetic derivative of bifendate, inhibits metastasis of triple-negative breast cancer via decreasing p38-regulated FOXC1 protein stability</title><author>Wang, Fan ; Liao, Rong ; Wang, Xin ; Xiong, Guixiang ; Zhang, Beibei ; Li, Juan ; Wu, Dengpan ; Chen, Yan ; Zhou, Xueyan ; Gu, Xiaoke ; Qi, Qi ; Li, Chenglin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c353t-875f5b42f34b38824b5dd1a9d06428da8948ae8fcf8bea3511bfb8987067dc373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Epithelial–mesenchymal transition</topic><topic>FOXC1 stability</topic><topic>Metastasis</topic><topic>N-3</topic><topic>P38</topic><topic>Triple-negative breast cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Fan</creatorcontrib><creatorcontrib>Liao, Rong</creatorcontrib><creatorcontrib>Wang, Xin</creatorcontrib><creatorcontrib>Xiong, Guixiang</creatorcontrib><creatorcontrib>Zhang, Beibei</creatorcontrib><creatorcontrib>Li, Juan</creatorcontrib><creatorcontrib>Wu, Dengpan</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Zhou, Xueyan</creatorcontrib><creatorcontrib>Gu, Xiaoke</creatorcontrib><creatorcontrib>Qi, Qi</creatorcontrib><creatorcontrib>Li, Chenglin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Fan</au><au>Liao, Rong</au><au>Wang, Xin</au><au>Xiong, Guixiang</au><au>Zhang, Beibei</au><au>Li, Juan</au><au>Wu, Dengpan</au><au>Chen, Yan</au><au>Zhou, Xueyan</au><au>Gu, Xiaoke</au><au>Qi, Qi</au><au>Li, Chenglin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>N-3, a novel synthetic derivative of bifendate, inhibits metastasis of triple-negative breast cancer via decreasing p38-regulated FOXC1 protein stability</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2023-09-01</date><risdate>2023</risdate><volume>215</volume><spage>115729</spage><epage>115729</epage><pages>115729-115729</pages><artnum>115729</artnum><issn>0006-2952</issn><eissn>1873-2968</eissn><abstract>[Display omitted]
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high invasiveness, metastatic potential, and poor prognosis. Epithelial–mesenchymal transition (EMT) is pivotal in TNBC progression, becoming a promising target for TNBC treatment. Our study evaluated N-3, a novel synthetic bifendate derivative, which inhibited the EMT-associated migration and invasion of MDA-MB-231 and 4T1 TNBC cells. The results were consistent with the suppression of FOXC1 expression and transcriptional activity. Additional studies indicated that N-3 reduced the protein stability of FOXC1 by enhancing ubiquitination and degradation. Moreover, N-3 downregulated p-p38 expression and FOXC1 interaction, decreasing the stability of p38-regulated FOXC1. Further, N-3 blocked TNBC metastasis with an artificial lung metastasis model in vivo, related to FOXC1 suppression and EMT. These results highlight the potential of N-3 as a TNBC metastasis treatment. Therefore, FOXC1 regulation could be a novel targeted therapeutic strategy for TNBC metastasis.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>37558004</pmid><doi>10.1016/j.bcp.2023.115729</doi><tpages>1</tpages></addata></record> |
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| subjects | Epithelial–mesenchymal transition FOXC1 stability Metastasis N-3 P38 Triple-negative breast cancer |
| title | N-3, a novel synthetic derivative of bifendate, inhibits metastasis of triple-negative breast cancer via decreasing p38-regulated FOXC1 protein stability |
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