TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma
The inositol polyphosphate kinase (IPK) family member ITPKA (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITPKA in malignancy disease and usually made...
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| Veröffentlicht in: | International journal of biological sciences 2020, Vol.16 (3), p.504-514 |
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| creator | Guoren, Zhou Zhaohui, Fan Wei, Zhu Mei, Wang Yuan, Wu Lin, Shi Xiaoyue, Xu Xiaomei, Zhang Bo, Shen |
| description | The inositol polyphosphate kinase (IPK) family member ITPKA (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITPKA in malignancy disease and usually made cancer more aggressive. However, the contribution of the inositol polyphosphate kinase ITPKA to lung cancer development remains unclear. Here we report that ITPKA is overexpressed in lung adenocarcinoma (LUAD) and positively correlated with advanced clinical parameters. ITPKA contributes to the malignant phenotypes
. Mechanistically, ITPKA executed its action through the inducting of epithelial-mesenchymal transition (EMT) and interacting with Drebrin 1 (which is related to cancer metastasis). Moreover, the hyper-expression of ITPKA in LUAD is transcriptionally activated by the transcription factor TFAP2A. In survival analysis by using tissue microarray (TMA), we indicate that ITPKA is hyper-expressed in LUAD tissues compared to adjacent normal tissues, and increased expression of ITPKA is associated with poor prognosis. Collectively, this study indicates that TFAP2A induced ITPKA hyperexpression promotes LUAD via interacting with Drebrin 1 and activating epithelial-mesenchymal transition (EMT). ITPKA might represent a potent candidate for the treatment and prognostic prediction of LUAD. |
| doi_str_mv | 10.7150/ijbs.40435 |
| format | Article |
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. Mechanistically, ITPKA executed its action through the inducting of epithelial-mesenchymal transition (EMT) and interacting with Drebrin 1 (which is related to cancer metastasis). Moreover, the hyper-expression of ITPKA in LUAD is transcriptionally activated by the transcription factor TFAP2A. In survival analysis by using tissue microarray (TMA), we indicate that ITPKA is hyper-expressed in LUAD tissues compared to adjacent normal tissues, and increased expression of ITPKA is associated with poor prognosis. Collectively, this study indicates that TFAP2A induced ITPKA hyperexpression promotes LUAD via interacting with Drebrin 1 and activating epithelial-mesenchymal transition (EMT). ITPKA might represent a potent candidate for the treatment and prognostic prediction of LUAD.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.40435</identifier><identifier>PMID: 32015686</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>1D-myo-Inositol-trisphosphate 3-kinase ; Adenocarcinoma ; Adenocarcinoma of Lung - genetics ; Adenocarcinoma of Lung - metabolism ; AP-2 protein ; Apoptosis ; Blotting, Western ; Cancer ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Movement - physiology ; Cell Proliferation - genetics ; Cell Proliferation - physiology ; Datasets ; DNA methylation ; DNA microarrays ; Epithelial-Mesenchymal Transition ; Flow Cytometry ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Gene Expression Regulation, Neoplastic - physiology ; Humans ; Immunohistochemistry ; Immunoprecipitation ; Inositol 1,4,5-trisphosphate receptors ; Inositol polyphosphate ; Kinases ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lymphatic system ; Malignancy ; Medical prognosis ; Mesenchyme ; Metastases ; Metastasis ; Neuropeptides - genetics ; Neuropeptides - metabolism ; Oncogenes ; Phenotypes ; Phosphotransferases (Alcohol Group Acceptor) - genetics ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Polyphosphate kinase ; Polyphosphates ; Protein Binding ; Proteins ; Research Paper ; Survival analysis ; Tissue analysis ; Tissues ; Transcription Factor AP-2 - genetics ; Transcription Factor AP-2 - metabolism ; Transcription factors ; Tumors ; Wound Healing - genetics ; Wound Healing - physiology</subject><ispartof>International journal of biological sciences, 2020, Vol.16 (3), p.504-514</ispartof><rights>The author(s).</rights><rights>Copyright Ivyspring International Publisher Pty Ltd 2020</rights><rights>2020. This work is published under https://creativecommons.org/licenses/by/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</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-6ba3055b170b4fa5e4ca4c9757645b723450de34500fb95f296245feb01a66523</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990902/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990902/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32015686$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guoren, Zhou</creatorcontrib><creatorcontrib>Zhaohui, Fan</creatorcontrib><creatorcontrib>Wei, Zhu</creatorcontrib><creatorcontrib>Mei, Wang</creatorcontrib><creatorcontrib>Yuan, Wu</creatorcontrib><creatorcontrib>Lin, Shi</creatorcontrib><creatorcontrib>Xiaoyue, Xu</creatorcontrib><creatorcontrib>Xiaomei, Zhang</creatorcontrib><creatorcontrib>Bo, Shen</creatorcontrib><title>TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>The inositol polyphosphate kinase (IPK) family member ITPKA (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITPKA in malignancy disease and usually made cancer more aggressive. However, the contribution of the inositol polyphosphate kinase ITPKA to lung cancer development remains unclear. Here we report that ITPKA is overexpressed in lung adenocarcinoma (LUAD) and positively correlated with advanced clinical parameters. ITPKA contributes to the malignant phenotypes
. Mechanistically, ITPKA executed its action through the inducting of epithelial-mesenchymal transition (EMT) and interacting with Drebrin 1 (which is related to cancer metastasis). Moreover, the hyper-expression of ITPKA in LUAD is transcriptionally activated by the transcription factor TFAP2A. In survival analysis by using tissue microarray (TMA), we indicate that ITPKA is hyper-expressed in LUAD tissues compared to adjacent normal tissues, and increased expression of ITPKA is associated with poor prognosis. Collectively, this study indicates that TFAP2A induced ITPKA hyperexpression promotes LUAD via interacting with Drebrin 1 and activating epithelial-mesenchymal transition (EMT). ITPKA might represent a potent candidate for the treatment and prognostic prediction of LUAD.</description><subject>1D-myo-Inositol-trisphosphate 3-kinase</subject><subject>Adenocarcinoma</subject><subject>Adenocarcinoma of Lung - genetics</subject><subject>Adenocarcinoma of Lung - metabolism</subject><subject>AP-2 protein</subject><subject>Apoptosis</subject><subject>Blotting, Western</subject><subject>Cancer</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - physiology</subject><subject>Cell Proliferation - genetics</subject><subject>Cell Proliferation - physiology</subject><subject>Datasets</subject><subject>DNA methylation</subject><subject>DNA microarrays</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Flow Cytometry</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Immunoprecipitation</subject><subject>Inositol 1,4,5-trisphosphate receptors</subject><subject>Inositol polyphosphate</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lymphatic system</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Neuropeptides - genetics</subject><subject>Neuropeptides - metabolism</subject><subject>Oncogenes</subject><subject>Phenotypes</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - genetics</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - metabolism</subject><subject>Polyphosphate kinase</subject><subject>Polyphosphates</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Research Paper</subject><subject>Survival analysis</subject><subject>Tissue analysis</subject><subject>Tissues</subject><subject>Transcription Factor AP-2 - genetics</subject><subject>Transcription Factor AP-2 - metabolism</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>Wound Healing - genetics</subject><subject>Wound Healing - physiology</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9kV1LHDEUhoNYqtXe9AeUgDdSWM33TG6E0XZ1cakLrhe9CpnMmXWW3USTmS39986oXawXhXBy4Dy8nMOD0BdKTjIqyWmzLNOJIILLHbRPhdAjxvJ8902_hz6ltCSEK5mTj2iPM0KlytU--jUfFzNW4ImvOgcVnsxn1wW-hbiBhG3_PL7xLizAQ9_3c99CtK5N-HfT3uPv5z8pbjyedn6Biwp8cDa6xoe1PUQfartK8Pn1P0B34x_zi6vR9OZyclFMR05w0Y5UaTmRsqQZKUVtJQhnhdOZzJSQZca4kKSCoZK61LJmWjEhaygJtUpJxg_Q2UvuQ1euoXLg22hX5iE2axv_mGAb8-_EN_dmETZGaU00GQKOXwNieOwgtWbdJAerlfUQumQYlz0nMj6gR-_QZeii788zTOpcUKq5_i_Fe2NSaaF66tsL5WJIKUK9XZkSM3g1g1fz7LWHv749cov-FcmfAHZDmq8</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Guoren, Zhou</creator><creator>Zhaohui, Fan</creator><creator>Wei, Zhu</creator><creator>Mei, Wang</creator><creator>Yuan, Wu</creator><creator>Lin, Shi</creator><creator>Xiaoyue, Xu</creator><creator>Xiaomei, Zhang</creator><creator>Bo, Shen</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2020</creationdate><title>TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma</title><author>Guoren, Zhou ; Zhaohui, Fan ; Wei, Zhu ; Mei, Wang ; Yuan, Wu ; Lin, Shi ; Xiaoyue, Xu ; Xiaomei, Zhang ; Bo, Shen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-6ba3055b170b4fa5e4ca4c9757645b723450de34500fb95f296245feb01a66523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1D-myo-Inositol-trisphosphate 3-kinase</topic><topic>Adenocarcinoma</topic><topic>Adenocarcinoma of Lung - genetics</topic><topic>Adenocarcinoma of Lung - metabolism</topic><topic>AP-2 protein</topic><topic>Apoptosis</topic><topic>Blotting, Western</topic><topic>Cancer</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - physiology</topic><topic>Cell Proliferation - genetics</topic><topic>Cell Proliferation - physiology</topic><topic>Datasets</topic><topic>DNA methylation</topic><topic>DNA microarrays</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Flow Cytometry</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Immunoprecipitation</topic><topic>Inositol 1,4,5-trisphosphate receptors</topic><topic>Inositol polyphosphate</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lymphatic system</topic><topic>Malignancy</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Neuropeptides - genetics</topic><topic>Neuropeptides - metabolism</topic><topic>Oncogenes</topic><topic>Phenotypes</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - genetics</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - metabolism</topic><topic>Polyphosphate kinase</topic><topic>Polyphosphates</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Research Paper</topic><topic>Survival analysis</topic><topic>Tissue analysis</topic><topic>Tissues</topic><topic>Transcription Factor AP-2 - genetics</topic><topic>Transcription Factor AP-2 - metabolism</topic><topic>Transcription factors</topic><topic>Tumors</topic><topic>Wound Healing - genetics</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guoren, Zhou</creatorcontrib><creatorcontrib>Zhaohui, Fan</creatorcontrib><creatorcontrib>Wei, Zhu</creatorcontrib><creatorcontrib>Mei, Wang</creatorcontrib><creatorcontrib>Yuan, Wu</creatorcontrib><creatorcontrib>Lin, Shi</creatorcontrib><creatorcontrib>Xiaoyue, Xu</creatorcontrib><creatorcontrib>Xiaomei, Zhang</creatorcontrib><creatorcontrib>Bo, Shen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Publicly Available Content (ProQuest)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guoren, Zhou</au><au>Zhaohui, Fan</au><au>Wei, Zhu</au><au>Mei, Wang</au><au>Yuan, Wu</au><au>Lin, Shi</au><au>Xiaoyue, Xu</au><au>Xiaomei, Zhang</au><au>Bo, Shen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2020</date><risdate>2020</risdate><volume>16</volume><issue>3</issue><spage>504</spage><epage>514</epage><pages>504-514</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>The inositol polyphosphate kinase (IPK) family member ITPKA (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITPKA in malignancy disease and usually made cancer more aggressive. However, the contribution of the inositol polyphosphate kinase ITPKA to lung cancer development remains unclear. Here we report that ITPKA is overexpressed in lung adenocarcinoma (LUAD) and positively correlated with advanced clinical parameters. ITPKA contributes to the malignant phenotypes
. Mechanistically, ITPKA executed its action through the inducting of epithelial-mesenchymal transition (EMT) and interacting with Drebrin 1 (which is related to cancer metastasis). Moreover, the hyper-expression of ITPKA in LUAD is transcriptionally activated by the transcription factor TFAP2A. In survival analysis by using tissue microarray (TMA), we indicate that ITPKA is hyper-expressed in LUAD tissues compared to adjacent normal tissues, and increased expression of ITPKA is associated with poor prognosis. Collectively, this study indicates that TFAP2A induced ITPKA hyperexpression promotes LUAD via interacting with Drebrin 1 and activating epithelial-mesenchymal transition (EMT). ITPKA might represent a potent candidate for the treatment and prognostic prediction of LUAD.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>32015686</pmid><doi>10.7150/ijbs.40435</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1D-myo-Inositol-trisphosphate 3-kinase Adenocarcinoma Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - metabolism AP-2 protein Apoptosis Blotting, Western Cancer Cell growth Cell Line, Tumor Cell Movement - genetics Cell Movement - physiology Cell Proliferation - genetics Cell Proliferation - physiology Datasets DNA methylation DNA microarrays Epithelial-Mesenchymal Transition Flow Cytometry Gene expression Gene Expression Regulation, Neoplastic - genetics Gene Expression Regulation, Neoplastic - physiology Humans Immunohistochemistry Immunoprecipitation Inositol 1,4,5-trisphosphate receptors Inositol polyphosphate Kinases Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Lymphatic system Malignancy Medical prognosis Mesenchyme Metastases Metastasis Neuropeptides - genetics Neuropeptides - metabolism Oncogenes Phenotypes Phosphotransferases (Alcohol Group Acceptor) - genetics Phosphotransferases (Alcohol Group Acceptor) - metabolism Polyphosphate kinase Polyphosphates Protein Binding Proteins Research Paper Survival analysis Tissue analysis Tissues Transcription Factor AP-2 - genetics Transcription Factor AP-2 - metabolism Transcription factors Tumors Wound Healing - genetics Wound Healing - physiology |
| title | TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma |
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