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Up‐regulation of plakophilin‐2 is correlated with the progression of glioma
Glioma is the most common type of primary brain tumor in the CNS. Due to its poor prognosis and high mortality rates, it is urgent to find out more effective therapies. Plakophilin‐2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migr...
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Published in: | Neuropathology 2017-06, Vol.37 (3), p.207-216 |
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creator | Zhang, Degeng Qian, Yuxia Liu, Xiaoxing Yu, Hong Zhao, Niangao Wu, Zhengdong |
description | Glioma is the most common type of primary brain tumor in the CNS. Due to its poor prognosis and high mortality rates, it is urgent to find out more effective therapies. Plakophilin‐2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migration of cancer cells and tumor progression has been shown. However, the expression and potential function of PKP2 in glioma was still unclear. In this study, we demonstrated that PKP2 protein expression level was increased in glioma tissues compared with normal brain tissues, and its level was significantly associated with the Ki‐67 expression and WHO grade by Western blot analysis and immunohistochemistry. Clinically, high PKP2 expression was tightly related to poor prognosis of glioma patients. Interestingly, we found that down‐regulated PKP2 expression was shown to inhibit the migration of cells in glioma. Moreover, cell counting kit (CCK)‐8 and colony formation analyses proved that reduced expression of PKP2 could weaken glioma cell proliferation. Taken together, these data uncover a potential role for PKP2 in the pathogenic process of glioma, suggesting that PKP2 may be a promising therapeutic target of glioma. |
doi_str_mv | 10.1111/neup.12363 |
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Due to its poor prognosis and high mortality rates, it is urgent to find out more effective therapies. Plakophilin‐2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migration of cancer cells and tumor progression has been shown. However, the expression and potential function of PKP2 in glioma was still unclear. In this study, we demonstrated that PKP2 protein expression level was increased in glioma tissues compared with normal brain tissues, and its level was significantly associated with the Ki‐67 expression and WHO grade by Western blot analysis and immunohistochemistry. Clinically, high PKP2 expression was tightly related to poor prognosis of glioma patients. Interestingly, we found that down‐regulated PKP2 expression was shown to inhibit the migration of cells in glioma. Moreover, cell counting kit (CCK)‐8 and colony formation analyses proved that reduced expression of PKP2 could weaken glioma cell proliferation. Taken together, these data uncover a potential role for PKP2 in the pathogenic process of glioma, suggesting that PKP2 may be a promising therapeutic target of glioma.</description><identifier>ISSN: 0919-6544</identifier><identifier>EISSN: 1440-1789</identifier><identifier>DOI: 10.1111/neup.12363</identifier><identifier>PMID: 28124385</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Adult ; Brain cancer ; Brain Neoplasms - genetics ; Brain Neoplasms - pathology ; Brain tumors ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Central nervous system ; Cholecystokinin ; Disease Progression ; Down-Regulation ; Female ; Glioma ; Glioma - genetics ; Glioma - pathology ; Glioma cells ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Ki-67 Antigen - metabolism ; Male ; Middle Aged ; migration ; Neoplasm Grading ; PKP2 ; Plakophilins - genetics ; Prognosis ; proliferation ; Up-Regulation</subject><ispartof>Neuropathology, 2017-06, Vol.37 (3), p.207-216</ispartof><rights>2017 Japanese Society of Neuropathology</rights><rights>2017 Japanese Society of Neuropathology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3813-268738c078bdbd054d70611e74cdd0872ee6c860f1af7b149c6611104d579b3b3</citedby><cites>FETCH-LOGICAL-c3813-268738c078bdbd054d70611e74cdd0872ee6c860f1af7b149c6611104d579b3b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28124385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Degeng</creatorcontrib><creatorcontrib>Qian, Yuxia</creatorcontrib><creatorcontrib>Liu, Xiaoxing</creatorcontrib><creatorcontrib>Yu, Hong</creatorcontrib><creatorcontrib>Zhao, Niangao</creatorcontrib><creatorcontrib>Wu, Zhengdong</creatorcontrib><title>Up‐regulation of plakophilin‐2 is correlated with the progression of glioma</title><title>Neuropathology</title><addtitle>Neuropathology</addtitle><description>Glioma is the most common type of primary brain tumor in the CNS. Due to its poor prognosis and high mortality rates, it is urgent to find out more effective therapies. Plakophilin‐2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migration of cancer cells and tumor progression has been shown. However, the expression and potential function of PKP2 in glioma was still unclear. In this study, we demonstrated that PKP2 protein expression level was increased in glioma tissues compared with normal brain tissues, and its level was significantly associated with the Ki‐67 expression and WHO grade by Western blot analysis and immunohistochemistry. Clinically, high PKP2 expression was tightly related to poor prognosis of glioma patients. Interestingly, we found that down‐regulated PKP2 expression was shown to inhibit the migration of cells in glioma. Moreover, cell counting kit (CCK)‐8 and colony formation analyses proved that reduced expression of PKP2 could weaken glioma cell proliferation. Taken together, these data uncover a potential role for PKP2 in the pathogenic process of glioma, suggesting that PKP2 may be a promising therapeutic target of glioma.</description><subject>Adult</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Central nervous system</subject><subject>Cholecystokinin</subject><subject>Disease Progression</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Glioma cells</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Male</subject><subject>Middle Aged</subject><subject>migration</subject><subject>Neoplasm Grading</subject><subject>PKP2</subject><subject>Plakophilins - genetics</subject><subject>Prognosis</subject><subject>proliferation</subject><subject>Up-Regulation</subject><issn>0919-6544</issn><issn>1440-1789</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kLtOwzAUhi0EoqWw8AAoEgtCSvFxnNgZUVUuUkUZ6Gzl4rQuSRzsRFU3HoFn5ElwSWFg4Cxn-L_z6-hD6BzwGNzc1LJrxkCCKDhAQ6AU-8B4fIiGOIbYj0JKB-jE2jXGwGLCj9GAcCA04OEQzRfN5_uHkcuuTFqla08XXlMmr7pZqVLVLiOesl6mjZGOkLm3Ue3Ka1fSa4xeGmnt_mpZKl0lp-ioSEorz_Z7hBZ305fJgz-b3z9Obmd-FnAIfBJxFvAMM57maY5DmjMcAUhGszzHnBEpo4xHuICkYCnQOItcDJjmIYvTIA1G6KrvdV-8ddK2olI2k2WZ1FJ3VgCPCOGEx8yhl3_Qte5M7b4TEGOKGThPjrruqcxoa40sRGNUlZitACx2msVOs_jW7OCLfWWXVjL_RX-8OgB6YKNKuf2nSjxNF8996RfuXIh2</recordid><startdate>201706</startdate><enddate>201706</enddate><creator>Zhang, Degeng</creator><creator>Qian, Yuxia</creator><creator>Liu, Xiaoxing</creator><creator>Yu, Hong</creator><creator>Zhao, Niangao</creator><creator>Wu, Zhengdong</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>7TK</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201706</creationdate><title>Up‐regulation of plakophilin‐2 is correlated with the progression of glioma</title><author>Zhang, Degeng ; Qian, Yuxia ; Liu, Xiaoxing ; Yu, Hong ; Zhao, Niangao ; Wu, Zhengdong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3813-268738c078bdbd054d70611e74cdd0872ee6c860f1af7b149c6611104d579b3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - pathology</topic><topic>Brain tumors</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Central nervous system</topic><topic>Cholecystokinin</topic><topic>Disease Progression</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Glioma cells</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Male</topic><topic>Middle Aged</topic><topic>migration</topic><topic>Neoplasm Grading</topic><topic>PKP2</topic><topic>Plakophilins - genetics</topic><topic>Prognosis</topic><topic>proliferation</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Degeng</creatorcontrib><creatorcontrib>Qian, Yuxia</creatorcontrib><creatorcontrib>Liu, Xiaoxing</creatorcontrib><creatorcontrib>Yu, Hong</creatorcontrib><creatorcontrib>Zhao, Niangao</creatorcontrib><creatorcontrib>Wu, Zhengdong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Degeng</au><au>Qian, Yuxia</au><au>Liu, Xiaoxing</au><au>Yu, Hong</au><au>Zhao, Niangao</au><au>Wu, Zhengdong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up‐regulation of plakophilin‐2 is correlated with the progression of glioma</atitle><jtitle>Neuropathology</jtitle><addtitle>Neuropathology</addtitle><date>2017-06</date><risdate>2017</risdate><volume>37</volume><issue>3</issue><spage>207</spage><epage>216</epage><pages>207-216</pages><issn>0919-6544</issn><eissn>1440-1789</eissn><abstract>Glioma is the most common type of primary brain tumor in the CNS. Due to its poor prognosis and high mortality rates, it is urgent to find out more effective therapies. Plakophilin‐2 (PKP2) is a widespread desmosomal plaque protein. Recently, the important roles of PKP2 in the proliferation and migration of cancer cells and tumor progression has been shown. However, the expression and potential function of PKP2 in glioma was still unclear. In this study, we demonstrated that PKP2 protein expression level was increased in glioma tissues compared with normal brain tissues, and its level was significantly associated with the Ki‐67 expression and WHO grade by Western blot analysis and immunohistochemistry. Clinically, high PKP2 expression was tightly related to poor prognosis of glioma patients. Interestingly, we found that down‐regulated PKP2 expression was shown to inhibit the migration of cells in glioma. Moreover, cell counting kit (CCK)‐8 and colony formation analyses proved that reduced expression of PKP2 could weaken glioma cell proliferation. 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subjects | Adult Brain cancer Brain Neoplasms - genetics Brain Neoplasms - pathology Brain tumors Cell Line, Tumor Cell Movement Cell Proliferation Central nervous system Cholecystokinin Disease Progression Down-Regulation Female Glioma Glioma - genetics Glioma - pathology Glioma cells Humans Immunohistochemistry Kaplan-Meier Estimate Ki-67 Antigen - metabolism Male Middle Aged migration Neoplasm Grading PKP2 Plakophilins - genetics Prognosis proliferation Up-Regulation |
title | Up‐regulation of plakophilin‐2 is correlated with the progression of glioma |
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