Silencing DEK downregulates cervical cancer tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/ p-Tyr216-GSK-3β/β-catenin axis
Cervical cancer is the second most common gynecological malignancy. The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hep...
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| Veröffentlicht in: | Oncology reports 2017-08, Vol.38 (2), p.1035-1042 |
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| creator | Xu, Xiaoyang Zou, Lin Yao, Qiuhui Zhang, Yanbo Gan, Li Tang, Liangdan |
| description | Cervical cancer is the second most common gynecological malignancy. The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hepatocellular cancer. However, its role in cervical cancer has not been well studied. In our study, we confirmed the DEK protein as an oncoprotein in cervical cancer tissues which is correlated to cervical cancer FIGO staging and tumor type. Moreover, in vitro loss of DEK inhibited cervical cancer cell proliferation, migration and invasion. We proved that silencing DEK downregulated Wnt/β-catenin and MMP-9, and silencing DEK increased GSK-3β activity via regulating its phosphorylation instead of translation. Silencing DEK reduced p-Ser9-GSK-3β and increased p-Tyr216-GSK-3β, which resulted in β-catenin degradation. Finally, the xenograft model in nude mice proved that silencing DEK impaired cervical cancer cell tumorigenicity. This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer. |
| doi_str_mv | 10.3892/or.2017.5721 |
| format | Article |
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The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hepatocellular cancer. However, its role in cervical cancer has not been well studied. In our study, we confirmed the DEK protein as an oncoprotein in cervical cancer tissues which is correlated to cervical cancer FIGO staging and tumor type. Moreover, in vitro loss of DEK inhibited cervical cancer cell proliferation, migration and invasion. We proved that silencing DEK downregulated Wnt/β-catenin and MMP-9, and silencing DEK increased GSK-3β activity via regulating its phosphorylation instead of translation. Silencing DEK reduced p-Ser9-GSK-3β and increased p-Tyr216-GSK-3β, which resulted in β-catenin degradation. Finally, the xenograft model in nude mice proved that silencing DEK impaired cervical cancer cell tumorigenicity. This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2017.5721</identifier><identifier>PMID: 28627610</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject><![CDATA[Adenocarcinoma - metabolism ; Adenocarcinoma - prevention & control ; Adenocarcinoma - secondary ; Animals ; Apoptosis ; beta Catenin - antagonists & inhibitors ; beta Catenin - genetics ; beta Catenin - metabolism ; Biomarkers, Tumor ; Bladder cancer ; Breast cancer ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - prevention & control ; Carcinoma, Squamous Cell - secondary ; Case-Control Studies ; Cell growth ; Cell Proliferation ; Cell Transformation, Neoplastic ; Cervical cancer ; Chromosomal Proteins, Non-Histone - antagonists & inhibitors ; Chromosomal Proteins, Non-Histone - genetics ; Chromosomal Proteins, Non-Histone - metabolism ; DEK ; Female ; Follow-Up Studies ; Gene Silencing ; Glycogen Synthase Kinase 3 beta - antagonists & inhibitors ; Glycogen Synthase Kinase 3 beta - genetics ; Glycogen Synthase Kinase 3 beta - metabolism ; GSK-3β ; Human papillomavirus ; Humans ; Kinases ; Leukemia ; Lymphatic Metastasis ; Medical research ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Invasiveness ; Oncogene Proteins - antagonists & inhibitors ; Oncogene Proteins - genetics ; Oncogene Proteins - metabolism ; Penicillin ; Phosphorylation ; Poly-ADP-Ribose Binding Proteins - antagonists & inhibitors ; Poly-ADP-Ribose Binding Proteins - genetics ; Poly-ADP-Ribose Binding Proteins - metabolism ; Prognosis ; Proteins ; Studies ; Transcription factors ; Tumor Cells, Cultured ; tumor metastasis ; Tumorigenesis ; Uterine Cervical Neoplasms - metabolism ; Uterine Cervical Neoplasms - pathology ; Uterine Cervical Neoplasms - prevention & control ; Wnt/β-catenin ; Xenograft Model Antitumor Assays]]></subject><ispartof>Oncology reports, 2017-08, Vol.38 (2), p.1035-1042</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-4ea763750ec83b56478e012bfff848bdbc18ea27446d39dc5ff04ef42b90b5a13</citedby><cites>FETCH-LOGICAL-c388t-4ea763750ec83b56478e012bfff848bdbc18ea27446d39dc5ff04ef42b90b5a13</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/28627610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Xiaoyang</creatorcontrib><creatorcontrib>Zou, Lin</creatorcontrib><creatorcontrib>Yao, Qiuhui</creatorcontrib><creatorcontrib>Zhang, Yanbo</creatorcontrib><creatorcontrib>Gan, Li</creatorcontrib><creatorcontrib>Tang, Liangdan</creatorcontrib><title>Silencing DEK downregulates cervical cancer tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/ p-Tyr216-GSK-3β/β-catenin axis</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Cervical cancer is the second most common gynecological malignancy. The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hepatocellular cancer. However, its role in cervical cancer has not been well studied. In our study, we confirmed the DEK protein as an oncoprotein in cervical cancer tissues which is correlated to cervical cancer FIGO staging and tumor type. Moreover, in vitro loss of DEK inhibited cervical cancer cell proliferation, migration and invasion. We proved that silencing DEK downregulated Wnt/β-catenin and MMP-9, and silencing DEK increased GSK-3β activity via regulating its phosphorylation instead of translation. Silencing DEK reduced p-Ser9-GSK-3β and increased p-Tyr216-GSK-3β, which resulted in β-catenin degradation. Finally, the xenograft model in nude mice proved that silencing DEK impaired cervical cancer cell tumorigenicity. This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer.</description><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - prevention & control</subject><subject>Adenocarcinoma - secondary</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>beta Catenin - antagonists & inhibitors</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Biomarkers, Tumor</subject><subject>Bladder cancer</subject><subject>Breast cancer</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - prevention & control</subject><subject>Carcinoma, Squamous Cell - secondary</subject><subject>Case-Control Studies</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic</subject><subject>Cervical cancer</subject><subject>Chromosomal Proteins, Non-Histone - antagonists & inhibitors</subject><subject>Chromosomal Proteins, Non-Histone - genetics</subject><subject>Chromosomal Proteins, Non-Histone - metabolism</subject><subject>DEK</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gene Silencing</subject><subject>Glycogen Synthase Kinase 3 beta - antagonists & inhibitors</subject><subject>Glycogen Synthase Kinase 3 beta - genetics</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>GSK-3β</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Kinases</subject><subject>Leukemia</subject><subject>Lymphatic Metastasis</subject><subject>Medical research</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Oncogene Proteins - antagonists & inhibitors</subject><subject>Oncogene Proteins - genetics</subject><subject>Oncogene Proteins - metabolism</subject><subject>Penicillin</subject><subject>Phosphorylation</subject><subject>Poly-ADP-Ribose Binding Proteins - antagonists & inhibitors</subject><subject>Poly-ADP-Ribose Binding Proteins - genetics</subject><subject>Poly-ADP-Ribose Binding Proteins - metabolism</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Studies</subject><subject>Transcription factors</subject><subject>Tumor Cells, Cultured</subject><subject>tumor metastasis</subject><subject>Tumorigenesis</subject><subject>Uterine Cervical Neoplasms - metabolism</subject><subject>Uterine Cervical Neoplasms - pathology</subject><subject>Uterine Cervical Neoplasms - prevention & control</subject><subject>Wnt/β-catenin</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNo9kN1KHDEUx0NpqV-967UECr1qdvM1k-RS1Nqi4MVa6N2QyZxZI7vJmMxYfQBfyAfxmcyyduHA-eDH_8APoa-MzoQ2fB7TjFOmZpXi7APaZ8owwqVgH8tMOSNCVH_30EHOd5RyRWvzGe1xXXNVM7qPnhd-BcH5sMRn55e4i_9CguW0siNk7CA9eGdX2NlQZjxO65j8EgJkn7ENHV7DaHOpsj54i8db2MTMB7KAZMjF4pKI15c5HsjNU-Ks3l1eX4grL4IP2D76fIQ-9XaV4ct7P0R_fp7fnP4iV9cXv09ProgTWo9EglW1UBUFp0Vb1VJpoIy3fd9rqduudUyD5UrKuhOmc1XfUwm95K2hbWWZOETftrlDivcT5LG5i1MK5WXDjJFGc86qQv3YUi7FnBP0zZD82qanhtFm47yJqdk4bzbOC378Hjq1a-h28H_JBfi-BfJQnPku5h0TExGaUE4KVok3l3iKcQ</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Xu, Xiaoyang</creator><creator>Zou, Lin</creator><creator>Yao, Qiuhui</creator><creator>Zhang, Yanbo</creator><creator>Gan, Li</creator><creator>Tang, Liangdan</creator><general>D.A. 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metabolism</topic><topic>Adenocarcinoma - prevention & control</topic><topic>Adenocarcinoma - secondary</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>beta Catenin - antagonists & inhibitors</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Biomarkers, Tumor</topic><topic>Bladder cancer</topic><topic>Breast cancer</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - prevention & control</topic><topic>Carcinoma, Squamous Cell - secondary</topic><topic>Case-Control Studies</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic</topic><topic>Cervical cancer</topic><topic>Chromosomal Proteins, Non-Histone - antagonists & inhibitors</topic><topic>Chromosomal Proteins, Non-Histone - genetics</topic><topic>Chromosomal Proteins, Non-Histone - metabolism</topic><topic>DEK</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gene Silencing</topic><topic>Glycogen Synthase Kinase 3 beta - antagonists & inhibitors</topic><topic>Glycogen Synthase Kinase 3 beta - genetics</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>GSK-3β</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Kinases</topic><topic>Leukemia</topic><topic>Lymphatic Metastasis</topic><topic>Medical research</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Oncogene Proteins - antagonists & inhibitors</topic><topic>Oncogene Proteins - genetics</topic><topic>Oncogene Proteins - metabolism</topic><topic>Penicillin</topic><topic>Phosphorylation</topic><topic>Poly-ADP-Ribose Binding Proteins - antagonists & inhibitors</topic><topic>Poly-ADP-Ribose Binding Proteins - genetics</topic><topic>Poly-ADP-Ribose Binding Proteins - metabolism</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Studies</topic><topic>Transcription factors</topic><topic>Tumor Cells, Cultured</topic><topic>tumor metastasis</topic><topic>Tumorigenesis</topic><topic>Uterine Cervical Neoplasms - 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The mechanisms of the genesis and progression of cervical cancer are complicated and not thoroughly understood. DEK is reported as an oncogene in various cancers, such as acute myeloid leukemia, bladder cancer, breast cancer and hepatocellular cancer. However, its role in cervical cancer has not been well studied. In our study, we confirmed the DEK protein as an oncoprotein in cervical cancer tissues which is correlated to cervical cancer FIGO staging and tumor type. Moreover, in vitro loss of DEK inhibited cervical cancer cell proliferation, migration and invasion. We proved that silencing DEK downregulated Wnt/β-catenin and MMP-9, and silencing DEK increased GSK-3β activity via regulating its phosphorylation instead of translation. Silencing DEK reduced p-Ser9-GSK-3β and increased p-Tyr216-GSK-3β, which resulted in β-catenin degradation. Finally, the xenograft model in nude mice proved that silencing DEK impaired cervical cancer cell tumorigenicity. This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28627610</pmid><doi>10.3892/or.2017.5721</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - metabolism Adenocarcinoma - prevention & control Adenocarcinoma - secondary Animals Apoptosis beta Catenin - antagonists & inhibitors beta Catenin - genetics beta Catenin - metabolism Biomarkers, Tumor Bladder cancer Breast cancer Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - prevention & control Carcinoma, Squamous Cell - secondary Case-Control Studies Cell growth Cell Proliferation Cell Transformation, Neoplastic Cervical cancer Chromosomal Proteins, Non-Histone - antagonists & inhibitors Chromosomal Proteins, Non-Histone - genetics Chromosomal Proteins, Non-Histone - metabolism DEK Female Follow-Up Studies Gene Silencing Glycogen Synthase Kinase 3 beta - antagonists & inhibitors Glycogen Synthase Kinase 3 beta - genetics Glycogen Synthase Kinase 3 beta - metabolism GSK-3β Human papillomavirus Humans Kinases Leukemia Lymphatic Metastasis Medical research Metastasis Mice Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Invasiveness Oncogene Proteins - antagonists & inhibitors Oncogene Proteins - genetics Oncogene Proteins - metabolism Penicillin Phosphorylation Poly-ADP-Ribose Binding Proteins - antagonists & inhibitors Poly-ADP-Ribose Binding Proteins - genetics Poly-ADP-Ribose Binding Proteins - metabolism Prognosis Proteins Studies Transcription factors Tumor Cells, Cultured tumor metastasis Tumorigenesis Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology Uterine Cervical Neoplasms - prevention & control Wnt/β-catenin Xenograft Model Antitumor Assays |
| title | Silencing DEK downregulates cervical cancer tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/ p-Tyr216-GSK-3β/β-catenin axis |
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