Roles of partitioning‐defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells
Summary A pivotal regulator of cell polarity and homeostasis, partitioning‐defective protein 6 (Par6) forms multicomponent complexes that not only regulate cell polarity and stabilize cell morphology, but have also been demonstrated to participate in the proliferation, migration and invasion of canc...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 2017-09, Vol.44 (9), p.909-913 |
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| container_title | Clinical and experimental pharmacology & physiology |
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| creator | Ruan, Lingling Shen, Yanting Lu, Ziwen Shang, Dongsheng Zhao, Zhicong Lu, Yongjin Wu, Yanfang Zhang, Yafei Tu, Zhigang Liu, Hanqing |
| description | Summary
A pivotal regulator of cell polarity and homeostasis, partitioning‐defective protein 6 (Par6) forms multicomponent complexes that not only regulate cell polarity and stabilize cell morphology, but have also been demonstrated to participate in the proliferation, migration and invasion of cancer cells. The transforming growth factor (TGF)‐β and extracellular signal‐regulated kinase (Erk) 1/2 pathways are the most thoroughly studied pathways involving Par6 in many cancers. Aurothiomalate has been used to disrupt the interaction between Par6 and atypical protein kinase C within the multicomponent complexes, and has been shown to effectively block transformed growth and metastasis in vitro and/or in vivo in a variety of cancers, including pancreatic, prostate and lung cancers, as well as alveolar rhabdomyosarcoma. It is likely that with further revelations regarding the critical roles of Par6 in cancer initiation, progression and metastasis, targeted therapies against Par6 will be discovered and prove effective preclinically, and hopefully clinically, in cancer treatment. |
| doi_str_mv | 10.1111/1440-1681.12794 |
| format | Article |
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A pivotal regulator of cell polarity and homeostasis, partitioning‐defective protein 6 (Par6) forms multicomponent complexes that not only regulate cell polarity and stabilize cell morphology, but have also been demonstrated to participate in the proliferation, migration and invasion of cancer cells. The transforming growth factor (TGF)‐β and extracellular signal‐regulated kinase (Erk) 1/2 pathways are the most thoroughly studied pathways involving Par6 in many cancers. Aurothiomalate has been used to disrupt the interaction between Par6 and atypical protein kinase C within the multicomponent complexes, and has been shown to effectively block transformed growth and metastasis in vitro and/or in vivo in a variety of cancers, including pancreatic, prostate and lung cancers, as well as alveolar rhabdomyosarcoma. It is likely that with further revelations regarding the critical roles of Par6 in cancer initiation, progression and metastasis, targeted therapies against Par6 will be discovered and prove effective preclinically, and hopefully clinically, in cancer treatment.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/1440-1681.12794</identifier><identifier>PMID: 28590507</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Adaptor Proteins, Signal Transducing - metabolism ; Alveoli ; Cancer ; Cell Movement ; cell polarization ; Cell Proliferation ; Cytology ; Enzyme Activation ; epithelial–mesenchymal transition ; Extracellular signal-regulated kinase ; Growth factors ; Homeostasis ; Humans ; Kinases ; Metastases ; Metastasis ; Morphology ; Neoplasm Invasiveness ; Neoplasms - metabolism ; Neoplasms - pathology ; Pancreas ; Partitioning ; partitioning‐defective protein 6 ; Polarity ; Prostate ; Protein kinase C ; Proteins ; Rhabdomyosarcoma ; transforming growth factor beta ; Transforming growth factor-b</subject><ispartof>Clinical and experimental pharmacology & physiology, 2017-09, Vol.44 (9), p.909-913</ispartof><rights>2017 John Wiley & Sons Australia, Ltd</rights><rights>2017 John Wiley & Sons Australia, Ltd.</rights><rights>Copyright © 2017 John Wiley & Sons Australia, Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4124-29eab896bdba4489f4ef92686c8cede99966067e51972a7d3a346021e86c71d23</citedby><cites>FETCH-LOGICAL-c4124-29eab896bdba4489f4ef92686c8cede99966067e51972a7d3a346021e86c71d23</cites><orcidid>0000-0001-7984-6305 ; 0000-0001-9844-3245</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1440-1681.12794$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1440-1681.12794$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28590507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ruan, Lingling</creatorcontrib><creatorcontrib>Shen, Yanting</creatorcontrib><creatorcontrib>Lu, Ziwen</creatorcontrib><creatorcontrib>Shang, Dongsheng</creatorcontrib><creatorcontrib>Zhao, Zhicong</creatorcontrib><creatorcontrib>Lu, Yongjin</creatorcontrib><creatorcontrib>Wu, Yanfang</creatorcontrib><creatorcontrib>Zhang, Yafei</creatorcontrib><creatorcontrib>Tu, Zhigang</creatorcontrib><creatorcontrib>Liu, Hanqing</creatorcontrib><title>Roles of partitioning‐defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells</title><title>Clinical and experimental pharmacology & physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>Summary
A pivotal regulator of cell polarity and homeostasis, partitioning‐defective protein 6 (Par6) forms multicomponent complexes that not only regulate cell polarity and stabilize cell morphology, but have also been demonstrated to participate in the proliferation, migration and invasion of cancer cells. The transforming growth factor (TGF)‐β and extracellular signal‐regulated kinase (Erk) 1/2 pathways are the most thoroughly studied pathways involving Par6 in many cancers. Aurothiomalate has been used to disrupt the interaction between Par6 and atypical protein kinase C within the multicomponent complexes, and has been shown to effectively block transformed growth and metastasis in vitro and/or in vivo in a variety of cancers, including pancreatic, prostate and lung cancers, as well as alveolar rhabdomyosarcoma. It is likely that with further revelations regarding the critical roles of Par6 in cancer initiation, progression and metastasis, targeted therapies against Par6 will be discovered and prove effective preclinically, and hopefully clinically, in cancer treatment.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Alveoli</subject><subject>Cancer</subject><subject>Cell Movement</subject><subject>cell polarization</subject><subject>Cell Proliferation</subject><subject>Cytology</subject><subject>Enzyme Activation</subject><subject>epithelial–mesenchymal transition</subject><subject>Extracellular signal-regulated kinase</subject><subject>Growth factors</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Kinases</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Morphology</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Pancreas</subject><subject>Partitioning</subject><subject>partitioning‐defective protein 6</subject><subject>Polarity</subject><subject>Prostate</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Rhabdomyosarcoma</subject><subject>transforming growth factor beta</subject><subject>Transforming growth factor-b</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctOxCAYhYnROONl7c6QuNHEzgCltCzNxFsyicbomjD074jpZYSOl52-gc_ok0in6sKNbPiB7xxOchDao2REwxpTzklERUZHlKWSr6Hh7806GpKYJBHNUjJAW94_EEISIuJNNGBZIsOcDtH7TVOCx02BF9q1trVNbev559tHDgWY1j4BXrimBVtjgQ-vtRNHWNc5tq3HpqkWJbwEeXht71dkaQtwurM5xpWd92OvqJ-07w7hL6NrAw4bKEu_gzYKXXrY_d630d3Z6e3kIppenV9OTqaR4ZTxiEnQs0yKWT7TnGey4FBIJjJhMgM5SCmFICKFhMqU6TSPdcwFYRQCkdKcxdvosPcNKR-X4FtVWd8l0DU0S6-oJJIKkbAkoAd_0Idm6eqQLlAsFXGScRKocU8Z13jvoFALZyvtXhUlqmtHdV2orgu1aico9r99l7MK8l_-p44AJD3wbEt4_c9PTU6ve-MvClWZ-A</recordid><startdate>201709</startdate><enddate>201709</enddate><creator>Ruan, Lingling</creator><creator>Shen, Yanting</creator><creator>Lu, Ziwen</creator><creator>Shang, Dongsheng</creator><creator>Zhao, Zhicong</creator><creator>Lu, Yongjin</creator><creator>Wu, Yanfang</creator><creator>Zhang, Yafei</creator><creator>Tu, Zhigang</creator><creator>Liu, Hanqing</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7984-6305</orcidid><orcidid>https://orcid.org/0000-0001-9844-3245</orcidid></search><sort><creationdate>201709</creationdate><title>Roles of partitioning‐defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells</title><author>Ruan, Lingling ; Shen, Yanting ; Lu, Ziwen ; Shang, Dongsheng ; Zhao, Zhicong ; Lu, Yongjin ; Wu, Yanfang ; Zhang, Yafei ; Tu, Zhigang ; Liu, Hanqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4124-29eab896bdba4489f4ef92686c8cede99966067e51972a7d3a346021e86c71d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Alveoli</topic><topic>Cancer</topic><topic>Cell Movement</topic><topic>cell polarization</topic><topic>Cell Proliferation</topic><topic>Cytology</topic><topic>Enzyme Activation</topic><topic>epithelial–mesenchymal transition</topic><topic>Extracellular signal-regulated kinase</topic><topic>Growth factors</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Kinases</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Morphology</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Pancreas</topic><topic>Partitioning</topic><topic>partitioning‐defective protein 6</topic><topic>Polarity</topic><topic>Prostate</topic><topic>Protein kinase C</topic><topic>Proteins</topic><topic>Rhabdomyosarcoma</topic><topic>transforming growth factor beta</topic><topic>Transforming growth factor-b</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ruan, Lingling</creatorcontrib><creatorcontrib>Shen, Yanting</creatorcontrib><creatorcontrib>Lu, Ziwen</creatorcontrib><creatorcontrib>Shang, Dongsheng</creatorcontrib><creatorcontrib>Zhao, Zhicong</creatorcontrib><creatorcontrib>Lu, Yongjin</creatorcontrib><creatorcontrib>Wu, Yanfang</creatorcontrib><creatorcontrib>Zhang, Yafei</creatorcontrib><creatorcontrib>Tu, Zhigang</creatorcontrib><creatorcontrib>Liu, Hanqing</creatorcontrib><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>Ruan, Lingling</au><au>Shen, Yanting</au><au>Lu, Ziwen</au><au>Shang, Dongsheng</au><au>Zhao, Zhicong</au><au>Lu, Yongjin</au><au>Wu, Yanfang</au><au>Zhang, Yafei</au><au>Tu, Zhigang</au><au>Liu, Hanqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of partitioning‐defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells</atitle><jtitle>Clinical and experimental pharmacology & physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2017-09</date><risdate>2017</risdate><volume>44</volume><issue>9</issue><spage>909</spage><epage>913</epage><pages>909-913</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>Summary
A pivotal regulator of cell polarity and homeostasis, partitioning‐defective protein 6 (Par6) forms multicomponent complexes that not only regulate cell polarity and stabilize cell morphology, but have also been demonstrated to participate in the proliferation, migration and invasion of cancer cells. The transforming growth factor (TGF)‐β and extracellular signal‐regulated kinase (Erk) 1/2 pathways are the most thoroughly studied pathways involving Par6 in many cancers. Aurothiomalate has been used to disrupt the interaction between Par6 and atypical protein kinase C within the multicomponent complexes, and has been shown to effectively block transformed growth and metastasis in vitro and/or in vivo in a variety of cancers, including pancreatic, prostate and lung cancers, as well as alveolar rhabdomyosarcoma. It is likely that with further revelations regarding the critical roles of Par6 in cancer initiation, progression and metastasis, targeted therapies against Par6 will be discovered and prove effective preclinically, and hopefully clinically, in cancer treatment.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28590507</pmid><doi>10.1111/1440-1681.12794</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0001-7984-6305</orcidid><orcidid>https://orcid.org/0000-0001-9844-3245</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - metabolism Alveoli Cancer Cell Movement cell polarization Cell Proliferation Cytology Enzyme Activation epithelial–mesenchymal transition Extracellular signal-regulated kinase Growth factors Homeostasis Humans Kinases Metastases Metastasis Morphology Neoplasm Invasiveness Neoplasms - metabolism Neoplasms - pathology Pancreas Partitioning partitioning‐defective protein 6 Polarity Prostate Protein kinase C Proteins Rhabdomyosarcoma transforming growth factor beta Transforming growth factor-b |
| title | Roles of partitioning‐defective protein 6 (Par6) and its complexes in the proliferation, migration and invasion of cancer cells |
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