α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation
Skin cutaneous melanoma (SKCM) is the skin malignancy with the highest mortality rate, and its morbidity rate is on the rise worldwide. Smoking is an independent marker of poor prognosis in melanoma. The α5-nicotinic acetylcholine receptor (α5-nAChR), one of the receptors for nicotine, is involved i...
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| Veröffentlicht in: | Archives of dermatological research 2024-05, Vol.316 (6), p.269, Article 269 |
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| creator | Li, Xiangying Meng, Xianguang Fan, Huiping Wang, Yan Jia, Yanfei Jiao, Jing Ma, Xiaoli |
| description | Skin cutaneous melanoma (SKCM) is the skin malignancy with the highest mortality rate, and its morbidity rate is on the rise worldwide. Smoking is an independent marker of poor prognosis in melanoma. The α5-nicotinic acetylcholine receptor (α5-nAChR), one of the receptors for nicotine, is involved in the proliferation, migration and invasion of SKCM cells. Nicotine has been reported to promote the expression of a disintegrin and metalloproteinase 10 (ADAM10), which is the key gene involved in melanoma progression. Here, we explored the link between α5-nAChR and ADAM10 in nicotine-associated cutaneous melanoma. α5-nAChR expression was correlated with ADAM10 expression and lower survival in SKCM. α5-nAChR mediated nicotine-induced ADAM10 expression via STAT3. The α5-nAChR/ADAM10 signaling axis was involved in the stemness and migration of SKCM cells. Furthermore, α5-nAChR expression was associated with ADAM10 expression, EMT marker expression and stemness marker expression in nicotine-related mice homograft tissues. These results suggest the role of the α5-nAChR/ADAM10 signaling pathway in nicotine-induced melanoma progression. |
| doi_str_mv | 10.1007/s00403-024-03110-0 |
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Smoking is an independent marker of poor prognosis in melanoma. The α5-nicotinic acetylcholine receptor (α5-nAChR), one of the receptors for nicotine, is involved in the proliferation, migration and invasion of SKCM cells. Nicotine has been reported to promote the expression of a disintegrin and metalloproteinase 10 (ADAM10), which is the key gene involved in melanoma progression. Here, we explored the link between α5-nAChR and ADAM10 in nicotine-associated cutaneous melanoma. α5-nAChR expression was correlated with ADAM10 expression and lower survival in SKCM. α5-nAChR mediated nicotine-induced ADAM10 expression via STAT3. The α5-nAChR/ADAM10 signaling axis was involved in the stemness and migration of SKCM cells. Furthermore, α5-nAChR expression was associated with ADAM10 expression, EMT marker expression and stemness marker expression in nicotine-related mice homograft tissues. These results suggest the role of the α5-nAChR/ADAM10 signaling pathway in nicotine-induced melanoma progression.</description><identifier>ISSN: 1432-069X</identifier><identifier>ISSN: 0340-3696</identifier><identifier>EISSN: 1432-069X</identifier><identifier>DOI: 10.1007/s00403-024-03110-0</identifier><identifier>PMID: 38795191</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acetylcholine receptors (nicotinic) ; ADAM10 Protein - genetics ; ADAM10 Protein - metabolism ; Amyloid Precursor Protein Secretases - genetics ; Amyloid Precursor Protein Secretases - metabolism ; Animals ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Dermatology ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; Male ; Malignancy ; Medical prognosis ; Medicine ; Medicine & Public Health ; Melanoma ; Melanoma - chemically induced ; Melanoma - metabolism ; Melanoma - pathology ; Melanoma, Cutaneous Malignant ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Morbidity ; Nicotine ; Nicotine - adverse effects ; Original Paper ; Receptors, Nicotinic - genetics ; Receptors, Nicotinic - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Skin cancer ; Skin Neoplasms - chemically induced ; Skin Neoplasms - metabolism ; Skin Neoplasms - pathology ; Stat3 protein ; STAT3 Transcription Factor - metabolism</subject><ispartof>Archives of dermatological research, 2024-05, Vol.316 (6), p.269, Article 269</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2024. 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The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-729e18554cbbfc609bbe6f3a2e780c21b5a5d21c232c57aca20bc3d848b933493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00403-024-03110-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00403-024-03110-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38795191$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xiangying</creatorcontrib><creatorcontrib>Meng, Xianguang</creatorcontrib><creatorcontrib>Fan, Huiping</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Jia, Yanfei</creatorcontrib><creatorcontrib>Jiao, Jing</creatorcontrib><creatorcontrib>Ma, Xiaoli</creatorcontrib><title>α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation</title><title>Archives of dermatological research</title><addtitle>Arch Dermatol Res</addtitle><addtitle>Arch Dermatol Res</addtitle><description>Skin cutaneous melanoma (SKCM) is the skin malignancy with the highest mortality rate, and its morbidity rate is on the rise worldwide. Smoking is an independent marker of poor prognosis in melanoma. The α5-nicotinic acetylcholine receptor (α5-nAChR), one of the receptors for nicotine, is involved in the proliferation, migration and invasion of SKCM cells. Nicotine has been reported to promote the expression of a disintegrin and metalloproteinase 10 (ADAM10), which is the key gene involved in melanoma progression. Here, we explored the link between α5-nAChR and ADAM10 in nicotine-associated cutaneous melanoma. α5-nAChR expression was correlated with ADAM10 expression and lower survival in SKCM. α5-nAChR mediated nicotine-induced ADAM10 expression via STAT3. The α5-nAChR/ADAM10 signaling axis was involved in the stemness and migration of SKCM cells. Furthermore, α5-nAChR expression was associated with ADAM10 expression, EMT marker expression and stemness marker expression in nicotine-related mice homograft tissues. These results suggest the role of the α5-nAChR/ADAM10 signaling pathway in nicotine-induced melanoma progression.</description><subject>Acetylcholine receptors (nicotinic)</subject><subject>ADAM10 Protein - genetics</subject><subject>ADAM10 Protein - metabolism</subject><subject>Amyloid Precursor Protein Secretases - genetics</subject><subject>Amyloid Precursor Protein Secretases - metabolism</subject><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Dermatology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Melanoma</subject><subject>Melanoma - chemically induced</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Melanoma, Cutaneous Malignant</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Morbidity</subject><subject>Nicotine</subject><subject>Nicotine - adverse effects</subject><subject>Original Paper</subject><subject>Receptors, Nicotinic - genetics</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Skin cancer</subject><subject>Skin Neoplasms - chemically induced</subject><subject>Skin Neoplasms - metabolism</subject><subject>Skin Neoplasms - pathology</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - metabolism</subject><issn>1432-069X</issn><issn>0340-3696</issn><issn>1432-069X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtOwzAQhi0EoqVwARYoEhs2pmM7iZNlVJ5SERIUiV3kOG7rKnWKnVTiWFyEM-GS8hALNh5r5pvf4_kROiZwTgD40AGEwDDQEAMjBDDsoD4JGcUQp8-7v-49dODcAnwTT8g-6rGEpxFJSR_N398ibLLR_GGYXWR3BAKnZ0ZU2syCpSq1aJQLjJZ1o43CVlU-UQaybYRRdes8UwlTL0WwsvXMKud0bYK1FsHjJJuwQMhGr0Xjk4dobyoqp462cYCeri4noxs8vr--HWVjLGkUN5jTVJEkikJZFFMZQ1oUKp4yQRVPQFJSRCIqKZGUURlxIQWFQrIyCZMiZSxM2QCddbp-oJdWuSZfaidVVXUD5wxiYJwmJPbo6R90UbfWf35Dcco54-GGoh0lbe2cVdN8ZfVS2NecQL7xIe98yL0P-acP_hygk610W_g1frd8Ld4DrAOcL5mZsj9v_yP7Ac3Ckuk</recordid><startdate>20240525</startdate><enddate>20240525</enddate><creator>Li, Xiangying</creator><creator>Meng, Xianguang</creator><creator>Fan, Huiping</creator><creator>Wang, Yan</creator><creator>Jia, Yanfei</creator><creator>Jiao, Jing</creator><creator>Ma, Xiaoli</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20240525</creationdate><title>α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation</title><author>Li, Xiangying ; Meng, Xianguang ; Fan, Huiping ; Wang, Yan ; Jia, Yanfei ; Jiao, Jing ; Ma, Xiaoli</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-729e18554cbbfc609bbe6f3a2e780c21b5a5d21c232c57aca20bc3d848b933493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acetylcholine receptors (nicotinic)</topic><topic>ADAM10 Protein - genetics</topic><topic>ADAM10 Protein - metabolism</topic><topic>Amyloid Precursor Protein Secretases - genetics</topic><topic>Amyloid Precursor Protein Secretases - metabolism</topic><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Dermatology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>Male</topic><topic>Malignancy</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Melanoma</topic><topic>Melanoma - chemically induced</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - pathology</topic><topic>Melanoma, Cutaneous Malignant</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Morbidity</topic><topic>Nicotine</topic><topic>Nicotine - adverse effects</topic><topic>Original Paper</topic><topic>Receptors, Nicotinic - genetics</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Skin cancer</topic><topic>Skin Neoplasms - chemically induced</topic><topic>Skin Neoplasms - metabolism</topic><topic>Skin Neoplasms - pathology</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xiangying</creatorcontrib><creatorcontrib>Meng, Xianguang</creatorcontrib><creatorcontrib>Fan, Huiping</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Jia, Yanfei</creatorcontrib><creatorcontrib>Jiao, Jing</creatorcontrib><creatorcontrib>Ma, Xiaoli</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of dermatological research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xiangying</au><au>Meng, Xianguang</au><au>Fan, Huiping</au><au>Wang, Yan</au><au>Jia, Yanfei</au><au>Jiao, Jing</au><au>Ma, Xiaoli</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation</atitle><jtitle>Archives of dermatological research</jtitle><stitle>Arch Dermatol Res</stitle><addtitle>Arch Dermatol Res</addtitle><date>2024-05-25</date><risdate>2024</risdate><volume>316</volume><issue>6</issue><spage>269</spage><pages>269-</pages><artnum>269</artnum><issn>1432-069X</issn><issn>0340-3696</issn><eissn>1432-069X</eissn><abstract>Skin cutaneous melanoma (SKCM) is the skin malignancy with the highest mortality rate, and its morbidity rate is on the rise worldwide. Smoking is an independent marker of poor prognosis in melanoma. The α5-nicotinic acetylcholine receptor (α5-nAChR), one of the receptors for nicotine, is involved in the proliferation, migration and invasion of SKCM cells. Nicotine has been reported to promote the expression of a disintegrin and metalloproteinase 10 (ADAM10), which is the key gene involved in melanoma progression. Here, we explored the link between α5-nAChR and ADAM10 in nicotine-associated cutaneous melanoma. α5-nAChR expression was correlated with ADAM10 expression and lower survival in SKCM. α5-nAChR mediated nicotine-induced ADAM10 expression via STAT3. The α5-nAChR/ADAM10 signaling axis was involved in the stemness and migration of SKCM cells. Furthermore, α5-nAChR expression was associated with ADAM10 expression, EMT marker expression and stemness marker expression in nicotine-related mice homograft tissues. These results suggest the role of the α5-nAChR/ADAM10 signaling pathway in nicotine-induced melanoma progression.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>38795191</pmid><doi>10.1007/s00403-024-03110-0</doi></addata></record> |
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| subjects | Acetylcholine receptors (nicotinic) ADAM10 Protein - genetics ADAM10 Protein - metabolism Amyloid Precursor Protein Secretases - genetics Amyloid Precursor Protein Secretases - metabolism Animals Cell Line, Tumor Cell migration Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Dermatology Disease Progression Female Gene Expression Regulation, Neoplastic - drug effects Humans Male Malignancy Medical prognosis Medicine Medicine & Public Health Melanoma Melanoma - chemically induced Melanoma - metabolism Melanoma - pathology Melanoma, Cutaneous Malignant Membrane Proteins - genetics Membrane Proteins - metabolism Mice Morbidity Nicotine Nicotine - adverse effects Original Paper Receptors, Nicotinic - genetics Receptors, Nicotinic - metabolism Signal transduction Signal Transduction - drug effects Skin cancer Skin Neoplasms - chemically induced Skin Neoplasms - metabolism Skin Neoplasms - pathology Stat3 protein STAT3 Transcription Factor - metabolism |
| title | α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation |
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