PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers
Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been...
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description | Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been evaluated in detail.
Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot.
PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result.
The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA. |
doi_str_mv | 10.1177/1533033820979681 |
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Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot.
PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result.
The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA.</description><identifier>ISSN: 1533-0346</identifier><identifier>EISSN: 1533-0338</identifier><identifier>DOI: 10.1177/1533033820979681</identifier><identifier>PMID: 33356974</identifier><language>eng</language><publisher>United States: Sage Publications Ltd</publisher><subject>Adult ; Aged ; Biomarkers, Tumor ; Cell cycle ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell Line, Tumor ; Cell lines ; Cell migration ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - genetics ; Cell survival ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cells, Cultured ; Cholangiocarcinoma ; Cholangiocarcinoma - etiology ; Cholangiocarcinoma - mortality ; Cholangiocarcinoma - pathology ; Clathrin ; Databases, Genetic ; Disease Progression ; Disease Susceptibility ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene set enrichment analysis ; Guanine Nucleotide Exchange Factors - genetics ; Guanine Nucleotide Exchange Factors - metabolism ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Male ; Medical prognosis ; Middle Aged ; mRNA ; Neoplasm Grading ; Neoplasm Staging ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Original ; Phosphatidylinositol ; Prognosis ; Proteins ; Tumors</subject><ispartof>Technology in cancer research & treatment, 2020-01, Vol.19, p.1533033820979681</ispartof><rights>The Author(s) 2020. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2020 2020 SAGE Publications</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-9978-7509</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7768323/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7768323/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33356974$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Zhao-Ming</creatorcontrib><creatorcontrib>Li, Hong-Bin</creatorcontrib><creatorcontrib>Chen, Shu-Guo</creatorcontrib><title>PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers</title><title>Technology in cancer research & treatment</title><addtitle>Technol Cancer Res Treat</addtitle><description>Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been evaluated in detail.
Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot.
PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result.
The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA.</description><subject>Adult</subject><subject>Aged</subject><subject>Biomarkers, Tumor</subject><subject>Cell cycle</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Cell survival</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cells, Cultured</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - etiology</subject><subject>Cholangiocarcinoma - mortality</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Clathrin</subject><subject>Databases, Genetic</subject><subject>Disease Progression</subject><subject>Disease Susceptibility</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene set enrichment analysis</subject><subject>Guanine Nucleotide Exchange Factors - genetics</subject><subject>Guanine Nucleotide Exchange Factors - metabolism</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Middle Aged</subject><subject>mRNA</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Staging</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Original</subject><subject>Phosphatidylinositol</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Tumors</subject><issn>1533-0346</issn><issn>1533-0338</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpVkc1OwzAQhC0E4v_OCVniSiD2NnZyQUKBAhKIqirnyEk3qcGNi51U6ovwvLhQEJzWmvF-u2MTcsLiC8akvGQJQAyQ8jiTmUjZFtlfS9Fa2_49D8QeOfD-NY65EMB2yR4AJCKTg33yMXp4Gt_enVNFn5R7Q0dtTUfOGl2jU5227Tkdqkob3akOPb1uGofe6yXSG1yisYs5tt26KZ9Zo9pG20q5Srd2rmiOxng6Uq4zKzqZOds3MzrGpjeB3DZfPs1XlcFojEHD6WYJf0R2amU8Hm_qIXkZ3k7y--jx-e4hv36MFgCii6oEk5BJMoVigFAJVpeQsCwbcF7XcZIKxUN-yFJWijKTKZZZKdW0Zii4lAiH5Oqbu-jLOU6rkMUpUyycniu3KqzSxX-n1bOisctCSpEChwA42wCcfe_Rd8Wr7V0bdi54IuPw5Cln4dbp3zG__J9_gE-GKYx2</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Jiang, Zhao-Ming</creator><creator>Li, Hong-Bin</creator><creator>Chen, Shu-Guo</creator><general>Sage Publications Ltd</general><general>SAGE Publications</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9978-7509</orcidid></search><sort><creationdate>20200101</creationdate><title>PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers</title><author>Jiang, Zhao-Ming ; Li, Hong-Bin ; Chen, Shu-Guo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p336t-c5e526671ae64e3c61fb35199422ff0586a20343981b6b978eb9b7adf1e6277e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biomarkers, Tumor</topic><topic>Cell cycle</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell lines</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Cell survival</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cells, Cultured</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - etiology</topic><topic>Cholangiocarcinoma - mortality</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Clathrin</topic><topic>Databases, Genetic</topic><topic>Disease Progression</topic><topic>Disease Susceptibility</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene set enrichment analysis</topic><topic>Guanine Nucleotide Exchange Factors - genetics</topic><topic>Guanine Nucleotide Exchange Factors - metabolism</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Middle Aged</topic><topic>mRNA</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Staging</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Original</topic><topic>Phosphatidylinositol</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Zhao-Ming</creatorcontrib><creatorcontrib>Li, Hong-Bin</creatorcontrib><creatorcontrib>Chen, Shu-Guo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Technology in cancer research & treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Zhao-Ming</au><au>Li, Hong-Bin</au><au>Chen, Shu-Guo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers</atitle><jtitle>Technology in cancer research & treatment</jtitle><addtitle>Technol Cancer Res Treat</addtitle><date>2020-01-01</date><risdate>2020</risdate><volume>19</volume><spage>1533033820979681</spage><pages>1533033820979681-</pages><issn>1533-0346</issn><eissn>1533-0338</eissn><abstract>Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) is a protein associated with cell proliferation. Its aberrant expression was reported to be correlated with the development in multiple tumors. However, its role in cholangiocarcinoma (CAA) has not yet been evaluated in detail.
Data were acquired from the public TCGA database for evaluating the expression pattern of PIMREG and assessing its clinical relevance as well as its correlation with overall survival. RBE and HUH28 cell lines were selected to perform loss- and gain-of-function of PIMREG assays respectively. Quantitative real-time PCR (RT-qPCR) and western blot analyses were used to measure the mRNA and protein levels of PIMREG. Cell Counting Kit-8, colony formation tests, and Transwell assays served to measure the effect of PIMREG on the proliferative, invasive and migratory capacities of CAA cells, appropriately. Gene set enrichment analysis (GSEA) was conducted to identify PIMREG associated gene set, which was further confirmed by western blot.
PIMREG was found to be highly expressed in CAA tissues and cell lines according to the public dataset and RT-qPCR analysis, and negatively related to the prognosis of patients with CAA. Moreover, knockdown of PIMREG suppressed and overexpression of PIMREG promoted the proliferation, invasion and migration of CAA cells. Furthermore, GSEA revealed that high PIMREG expression was positively associated with cell cycle signaling. And the next western blot analysis demonstrated that silencing PIMREG resulted in a reduction on the levels of p-CDK1, CCNE1, and CCNB1, whereas PIMREG overexpression led to an opposite result.
The results suggested that PIMREG facilitates the growth, invasion and migration of CAA cells partly by regulating the cell cycle relative biomarkers, revealing that PIMREG may be a crucial molecule in the progression of CAA.</abstract><cop>United States</cop><pub>Sage Publications Ltd</pub><pmid>33356974</pmid><doi>10.1177/1533033820979681</doi><orcidid>https://orcid.org/0000-0001-9978-7509</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Biomarkers, Tumor Cell cycle Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Line, Tumor Cell lines Cell migration Cell Movement - genetics Cell proliferation Cell Proliferation - genetics Cell survival Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cells, Cultured Cholangiocarcinoma Cholangiocarcinoma - etiology Cholangiocarcinoma - mortality Cholangiocarcinoma - pathology Clathrin Databases, Genetic Disease Progression Disease Susceptibility Female Gene Expression Profiling Gene Expression Regulation, Neoplastic Gene set enrichment analysis Guanine Nucleotide Exchange Factors - genetics Guanine Nucleotide Exchange Factors - metabolism Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Male Medical prognosis Middle Aged mRNA Neoplasm Grading Neoplasm Staging Nuclear Proteins - genetics Nuclear Proteins - metabolism Original Phosphatidylinositol Prognosis Proteins Tumors |
title | PIMREG, a Marker of Proliferation, Facilitates Aggressive Development of Cholangiocarcinoma Cells Partly Through Regulating Cell Cycle-Related Markers |
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