Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis
Background Exosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in re...
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| Veröffentlicht in: | Breast cancer (Tokyo, Japan) Japan), 2023-11, Vol.30 (6), p.1028-1040 |
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| creator | Dong, Huaying Yang, Changcheng Chen, Xiang Sun, Hening He, Xionghui Wang, Wei |
| description | Background
Exosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in regulating CAFs transformation.
Methods
Adjacent normal tissues, cancerous and serum specimens were gathered in breast cancer patients. Exosomes and NFs were separated from breast cancer cells (SKBR-3) and normal tissues of patients, respectively. Cell viability and migration were measured with CCK-8 and Transwell assays. CAFs markers, fibroblast activation protein (FAP) and a-smooth muscle actin (α-SMA) were detected for assessing CAFs activation. The interactions between molecules were evaluated using dual luciferase reporter assay, RNA immunoprecipitation and chromatin immunoprecipitation.
Results
SNHG14 and FAM171A1 were upregulated in breast cancer. Exosomes secreted by SKBR-3 cells induced NFs activation in CAFs, as indicated by upregulating CAFs marker levels and facilitated cell viability and migration. Exosomal SNHG14 silencing in SKBR-3 cells inhibited CAFs activation. SNHG14 positively regulated FAM171A1 expression through EBF1. FAM171A1 overexpression eliminated the inhibition effect of exosomal SNHG14 silencing in CAFs transformation.
Conclusion
Breast cancer-derived exosomal SNHG14 contributed to NFs transformation into CAFs by the EBF1/FAM171A1 axis. |
| doi_str_mv | 10.1007/s12282-023-01496-9 |
| format | Article |
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Exosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in regulating CAFs transformation.
Methods
Adjacent normal tissues, cancerous and serum specimens were gathered in breast cancer patients. Exosomes and NFs were separated from breast cancer cells (SKBR-3) and normal tissues of patients, respectively. Cell viability and migration were measured with CCK-8 and Transwell assays. CAFs markers, fibroblast activation protein (FAP) and a-smooth muscle actin (α-SMA) were detected for assessing CAFs activation. The interactions between molecules were evaluated using dual luciferase reporter assay, RNA immunoprecipitation and chromatin immunoprecipitation.
Results
SNHG14 and FAM171A1 were upregulated in breast cancer. Exosomes secreted by SKBR-3 cells induced NFs activation in CAFs, as indicated by upregulating CAFs marker levels and facilitated cell viability and migration. Exosomal SNHG14 silencing in SKBR-3 cells inhibited CAFs activation. SNHG14 positively regulated FAM171A1 expression through EBF1. FAM171A1 overexpression eliminated the inhibition effect of exosomal SNHG14 silencing in CAFs transformation.
Conclusion
Breast cancer-derived exosomal SNHG14 contributed to NFs transformation into CAFs by the EBF1/FAM171A1 axis.</description><identifier>ISSN: 1340-6868</identifier><identifier>EISSN: 1880-4233</identifier><identifier>DOI: 10.1007/s12282-023-01496-9</identifier><language>eng</language><publisher>Singapore: Springer Nature Singapore</publisher><subject>Breast cancer ; Cancer Research ; Development and progression ; Medicine ; Medicine & Public Health ; Muscle proteins ; Oncology ; Original Article ; RNA ; Surgery ; Surgical Oncology</subject><ispartof>Breast cancer (Tokyo, Japan), 2023-11, Vol.30 (6), p.1028-1040</ispartof><rights>The Author(s), under exclusive licence to The Japanese Breast Cancer Society 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>COPYRIGHT 2023 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-7aa22327ddd94dad4cc13d67cae01a9b3d04dcfa8a47d9aa4849c590ab67ef3c3</citedby><cites>FETCH-LOGICAL-c391t-7aa22327ddd94dad4cc13d67cae01a9b3d04dcfa8a47d9aa4849c590ab67ef3c3</cites><orcidid>0000-0002-4905-6940</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12282-023-01496-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12282-023-01496-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids></links><search><creatorcontrib>Dong, Huaying</creatorcontrib><creatorcontrib>Yang, Changcheng</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Sun, Hening</creatorcontrib><creatorcontrib>He, Xionghui</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><title>Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis</title><title>Breast cancer (Tokyo, Japan)</title><addtitle>Breast Cancer</addtitle><description>Background
Exosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in regulating CAFs transformation.
Methods
Adjacent normal tissues, cancerous and serum specimens were gathered in breast cancer patients. Exosomes and NFs were separated from breast cancer cells (SKBR-3) and normal tissues of patients, respectively. Cell viability and migration were measured with CCK-8 and Transwell assays. CAFs markers, fibroblast activation protein (FAP) and a-smooth muscle actin (α-SMA) were detected for assessing CAFs activation. The interactions between molecules were evaluated using dual luciferase reporter assay, RNA immunoprecipitation and chromatin immunoprecipitation.
Results
SNHG14 and FAM171A1 were upregulated in breast cancer. Exosomes secreted by SKBR-3 cells induced NFs activation in CAFs, as indicated by upregulating CAFs marker levels and facilitated cell viability and migration. Exosomal SNHG14 silencing in SKBR-3 cells inhibited CAFs activation. SNHG14 positively regulated FAM171A1 expression through EBF1. FAM171A1 overexpression eliminated the inhibition effect of exosomal SNHG14 silencing in CAFs transformation.
Conclusion
Breast cancer-derived exosomal SNHG14 contributed to NFs transformation into CAFs by the EBF1/FAM171A1 axis.</description><subject>Breast cancer</subject><subject>Cancer Research</subject><subject>Development and progression</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Muscle proteins</subject><subject>Oncology</subject><subject>Original Article</subject><subject>RNA</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><issn>1340-6868</issn><issn>1880-4233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kU1rFTEUhgdRsFb_gKuAGzdp89VkspyW3rZQK_ixDucmZ2rK3KQmcy_tj_A_m9tRRBDJ4oTked7FebvuLWdHnDFzXLkQvaBMSMq4spraZ90B73tGlZDyebtLxajudf-ye1XrHWNKGqYPuh-nBaHOxEPyWGjAEncYCD7kmjcwkSn5TzcD-XxzecEViSlsPVaSctl_jnFd8nra--DnuIM55kTm_DsNas0-wtwC_6CV7CKQ-RuS89MVP14NH7jhAyfwEOvr7sUIU8U3v-Zh93V1_uXskl5_vLg6G66pl5bP1AAIIYUJIVgVICjvuQzaeEDGwa5lYCr4EXpQJlgA1SvrTyyDtTY4Si8Pu_dL7n3J37dYZ7eJ1eM0QcK8rU70minGuVINfbegtzChi2nMcwG_x91gtNXyhGvTqKN_UO0E3ESfE46xvf8liEXwJddacHT3JW6gPDrO3L5St1TqWqXuqVJnmyQXqTY43WJxd3lbUtvU_6yfE3Kj6w</recordid><startdate>20231101</startdate><enddate>20231101</enddate><creator>Dong, Huaying</creator><creator>Yang, Changcheng</creator><creator>Chen, Xiang</creator><creator>Sun, Hening</creator><creator>He, Xionghui</creator><creator>Wang, Wei</creator><general>Springer Nature Singapore</general><general>Springer</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4905-6940</orcidid></search><sort><creationdate>20231101</creationdate><title>Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis</title><author>Dong, Huaying ; Yang, Changcheng ; Chen, Xiang ; Sun, Hening ; He, Xionghui ; Wang, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-7aa22327ddd94dad4cc13d67cae01a9b3d04dcfa8a47d9aa4849c590ab67ef3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Breast cancer</topic><topic>Cancer Research</topic><topic>Development and progression</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Muscle proteins</topic><topic>Oncology</topic><topic>Original Article</topic><topic>RNA</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Huaying</creatorcontrib><creatorcontrib>Yang, Changcheng</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Sun, Hening</creatorcontrib><creatorcontrib>He, Xionghui</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Breast cancer (Tokyo, Japan)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dong, Huaying</au><au>Yang, Changcheng</au><au>Chen, Xiang</au><au>Sun, Hening</au><au>He, Xionghui</au><au>Wang, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis</atitle><jtitle>Breast cancer (Tokyo, Japan)</jtitle><stitle>Breast Cancer</stitle><date>2023-11-01</date><risdate>2023</risdate><volume>30</volume><issue>6</issue><spage>1028</spage><epage>1040</epage><pages>1028-1040</pages><issn>1340-6868</issn><eissn>1880-4233</eissn><abstract>Background
Exosomes released from cancer cells can activate normal fibroblasts (NFs) into cancer-associated fibroblasts (CAFs), which promotes cancer development. Our study aims to explore the role and potential mechanisms of breast cancer exosomes-delivered long non-coding RNA (lncRNA) SNHG14 in regulating CAFs transformation.
Methods
Adjacent normal tissues, cancerous and serum specimens were gathered in breast cancer patients. Exosomes and NFs were separated from breast cancer cells (SKBR-3) and normal tissues of patients, respectively. Cell viability and migration were measured with CCK-8 and Transwell assays. CAFs markers, fibroblast activation protein (FAP) and a-smooth muscle actin (α-SMA) were detected for assessing CAFs activation. The interactions between molecules were evaluated using dual luciferase reporter assay, RNA immunoprecipitation and chromatin immunoprecipitation.
Results
SNHG14 and FAM171A1 were upregulated in breast cancer. Exosomes secreted by SKBR-3 cells induced NFs activation in CAFs, as indicated by upregulating CAFs marker levels and facilitated cell viability and migration. Exosomal SNHG14 silencing in SKBR-3 cells inhibited CAFs activation. SNHG14 positively regulated FAM171A1 expression through EBF1. FAM171A1 overexpression eliminated the inhibition effect of exosomal SNHG14 silencing in CAFs transformation.
Conclusion
Breast cancer-derived exosomal SNHG14 contributed to NFs transformation into CAFs by the EBF1/FAM171A1 axis.</abstract><cop>Singapore</cop><pub>Springer Nature Singapore</pub><doi>10.1007/s12282-023-01496-9</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4905-6940</orcidid></addata></record> |
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| subjects | Breast cancer Cancer Research Development and progression Medicine Medicine & Public Health Muscle proteins Oncology Original Article RNA Surgery Surgical Oncology |
| title | Breast cancer-derived exosomal lncRNA SNHG14 induces normal fibroblast activation to cancer-associated fibroblasts via the EBF1/FAM171A1 axis |
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