ER stress-induced autophagy in melanoma
Summary The activation of RAF‐MEK–extracellular signal‐regulated kinase (ERK) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 (BRAF)V600E mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 2015-08, Vol.42 (8), p.811-816 |
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| container_title | Clinical and experimental pharmacology & physiology |
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| creator | Meng, Xiao-Xiao Yao, Mu Zhang, Xu Dong Xu, Hong-Xi Dong, Qihan |
| description | Summary
The activation of RAF‐MEK–extracellular signal‐regulated kinase (ERK) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 (BRAF)V600E mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the positive response to BRAFi is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAFi. There is growing evidence to suggest that endoplasmic reticulum (ER) stress‐induced autophagy could be a potential pro‐survival mechanism that contributes to genesis of melanoma and to the resistance to BRAFi. ER stress‐induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAFi‐resistant melanoma. |
| doi_str_mv | 10.1111/1440-1681.12436 |
| format | Article |
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The activation of RAF‐MEK–extracellular signal‐regulated kinase (ERK) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 (BRAF)V600E mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the positive response to BRAFi is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAFi. There is growing evidence to suggest that endoplasmic reticulum (ER) stress‐induced autophagy could be a potential pro‐survival mechanism that contributes to genesis of melanoma and to the resistance to BRAFi. ER stress‐induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAFi‐resistant melanoma.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/1440-1681.12436</identifier><identifier>PMID: 26096022</identifier><language>eng</language><publisher>Australia: Blackwell Publishing Ltd</publisher><subject>Animals ; Autophagy ; BRAFi resistant melanoma ; Endoplasmic Reticulum Stress ; ER stress ; Humans ; Kinases ; melanocytic nevus ; Melanoma ; Melanoma - metabolism ; Melanoma - pathology ; primary and metastatic melanoma</subject><ispartof>Clinical and experimental pharmacology & physiology, 2015-08, Vol.42 (8), p.811-816</ispartof><rights>2015 Wiley Publishing Asia Pty Ltd</rights><rights>2015 Wiley Publishing Asia Pty Ltd.</rights><rights>Copyright © 2015 Wiley Publishing Asia Pty Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4756-91c0e29d681e5868fba4abd393d07bce2b9f9ad370c29ce01b2f0cd55eec07413</citedby><cites>FETCH-LOGICAL-c4756-91c0e29d681e5868fba4abd393d07bce2b9f9ad370c29ce01b2f0cd55eec07413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1440-1681.12436$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1440-1681.12436$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26096022$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Meng, Xiao-Xiao</creatorcontrib><creatorcontrib>Yao, Mu</creatorcontrib><creatorcontrib>Zhang, Xu Dong</creatorcontrib><creatorcontrib>Xu, Hong-Xi</creatorcontrib><creatorcontrib>Dong, Qihan</creatorcontrib><title>ER stress-induced autophagy in melanoma</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>Summary
The activation of RAF‐MEK–extracellular signal‐regulated kinase (ERK) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 (BRAF)V600E mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the positive response to BRAFi is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAFi. There is growing evidence to suggest that endoplasmic reticulum (ER) stress‐induced autophagy could be a potential pro‐survival mechanism that contributes to genesis of melanoma and to the resistance to BRAFi. ER stress‐induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAFi‐resistant melanoma.</description><subject>Animals</subject><subject>Autophagy</subject><subject>BRAFi resistant melanoma</subject><subject>Endoplasmic Reticulum Stress</subject><subject>ER stress</subject><subject>Humans</subject><subject>Kinases</subject><subject>melanocytic nevus</subject><subject>Melanoma</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>primary and metastatic melanoma</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1PwzAQhi0EoqUws6FKDLCkPduxHY-oKi2iAsRXR8txLpDSNCVuBP33pPRjYMHLSdbzvnd6CDml0KH169IwhIDKiHYoC7ncI83dzz5pAgcR0EhBgxx5PwEAAZIfkgaToCUw1iQX_ce2X5TofZDNksph0rbVopi_27dlO5u1c5zaWZHbY3KQ2qnHk81skZfr_nNvGIzuBze9q1HgQiVkoKkDZDqp96OIZJTGNrRxwjVPQMUOWaxTbROuwDHtEGjMUnCJEIgOVEh5i1yue-dl8VmhX5g88w6n9RVYVN5QBSAjrkHU6PkfdFJU5ay-zlCpNVdS13tbpLumXFl4X2Jq5mWW23JpKJiVQ7MyZlbGzK_DOnG26a3iHJMdv5VWA2INfGVTXP7XZ3r9h21xsM5lfoHfu5wtP4xUXAkzvhuYQe9WvT6xoRnzH91Yh_M</recordid><startdate>201508</startdate><enddate>201508</enddate><creator>Meng, Xiao-Xiao</creator><creator>Yao, Mu</creator><creator>Zhang, Xu Dong</creator><creator>Xu, Hong-Xi</creator><creator>Dong, Qihan</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>7QP</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope></search><sort><creationdate>201508</creationdate><title>ER stress-induced autophagy in melanoma</title><author>Meng, Xiao-Xiao ; Yao, Mu ; Zhang, Xu Dong ; Xu, Hong-Xi ; Dong, Qihan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4756-91c0e29d681e5868fba4abd393d07bce2b9f9ad370c29ce01b2f0cd55eec07413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Autophagy</topic><topic>BRAFi resistant melanoma</topic><topic>Endoplasmic Reticulum Stress</topic><topic>ER stress</topic><topic>Humans</topic><topic>Kinases</topic><topic>melanocytic nevus</topic><topic>Melanoma</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - pathology</topic><topic>primary and metastatic melanoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Meng, Xiao-Xiao</creatorcontrib><creatorcontrib>Yao, Mu</creatorcontrib><creatorcontrib>Zhang, Xu Dong</creatorcontrib><creatorcontrib>Xu, Hong-Xi</creatorcontrib><creatorcontrib>Dong, Qihan</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental pharmacology & physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Meng, Xiao-Xiao</au><au>Yao, Mu</au><au>Zhang, Xu Dong</au><au>Xu, Hong-Xi</au><au>Dong, Qihan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ER stress-induced autophagy in melanoma</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2015-08</date><risdate>2015</risdate><volume>42</volume><issue>8</issue><spage>811</spage><epage>816</epage><pages>811-816</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>Summary
The activation of RAF‐MEK–extracellular signal‐regulated kinase (ERK) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 (BRAF)V600E mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the positive response to BRAFi is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAFi. There is growing evidence to suggest that endoplasmic reticulum (ER) stress‐induced autophagy could be a potential pro‐survival mechanism that contributes to genesis of melanoma and to the resistance to BRAFi. ER stress‐induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAFi‐resistant melanoma.</abstract><cop>Australia</cop><pub>Blackwell Publishing Ltd</pub><pmid>26096022</pmid><doi>10.1111/1440-1681.12436</doi><tpages>6</tpages></addata></record> |
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| ispartof | Clinical and experimental pharmacology & physiology, 2015-08, Vol.42 (8), p.811-816 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Autophagy BRAFi resistant melanoma Endoplasmic Reticulum Stress ER stress Humans Kinases melanocytic nevus Melanoma Melanoma - metabolism Melanoma - pathology primary and metastatic melanoma |
| title | ER stress-induced autophagy in melanoma |
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