DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway
Background Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear. Patients and Methods Eighty-seven patients with ESCC were enrolled in...
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| Veröffentlicht in: | Annals of surgical oncology 2020-06, Vol.27 (6), p.2090-2101 |
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| container_title | Annals of surgical oncology |
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| creator | Chiu, Wen-Chin Fang, Pen-Tzu Lee, Yi-Chen Wang, Yen-Yun Su, Yu-Han Hu, Stephen Chu-Sung Chen, Yuk-Kwan Tsui, Yu-Tong Kao, Ying-Hsien Huang, Ming-Yii Yuan, Shyng-Shiou F. |
| description | Background
Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear.
Patients and Methods
Eighty-seven patients with ESCC were enrolled in this study. Expression of Rad51 in ESCC was determined by immunohistochemistry and correlated with clinicopathological variables by Chi square test. The role of Rad51 in patient survival was determined by Kaplan–Meier estimates. The effects of Rad51 knockdown and overexpression on esophageal cancer growth, migration, and invasion were examined using TE8, CE81T, and KYSE70 cells. The mechanisms involved were also analyzed. Nude mice models were used for assessment of tumor growth.
Results
Rad51 staining was predominantly observed in ESCC patients. ESCC patients with high Rad51 expression had significantly decreased survival (
P
|
| doi_str_mv | 10.1245/s10434-019-08043-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2400057721</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2400057721</sourcerecordid><originalsourceid>FETCH-LOGICAL-c441t-9da030a34bcf270741d1777fc83e79c22eef14ac91c08961aedde121db0a527a3</originalsourceid><addsrcrecordid>eNp9kE1P3DAQhi1EVT7aP8ChssQ5xWM76-S4WihFoi0CerZm7QkbuomDnRS48ssxLG1vlSx5ZD_vO9LD2AGIzyB1eZRAaKULAXUhqjwWD1tsF8r8pGcVbOdZzKqilrNyh-2ldCsEGCXK92xHgdF1zuyyp-Pvc35JA7aRX8QwUtvzS_Ql8LPeT44Sv566EPlpDPfjimPv-TcaMeXTJp7hkxSGFd4QrvnV3YRdmBJf0HrNFxhd24cO-e8WOfJBVUfzX2NxTAP1nvqRX-C4usfHD-xdg-tEH9_uffbzy8n14mtx_uP0bDE_L5zWMBa1R6EEKr10jTTCaPBgjGlcpcjUTkqiBjS6Gpyo6hkgeU8gwS8FltKg2meHm94hhruJ0mhvwxT7vNJKLYQojZGQKbmhXAwpRWrsENsO46MFYV-02412m7XbV-32IYc-vVVPy47838gfzxlQGyDlr_6G4r_d_6l9BqB_jbI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2400057721</pqid></control><display><type>article</type><title>DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Chiu, Wen-Chin ; Fang, Pen-Tzu ; Lee, Yi-Chen ; Wang, Yen-Yun ; Su, Yu-Han ; Hu, Stephen Chu-Sung ; Chen, Yuk-Kwan ; Tsui, Yu-Tong ; Kao, Ying-Hsien ; Huang, Ming-Yii ; Yuan, Shyng-Shiou F.</creator><creatorcontrib>Chiu, Wen-Chin ; Fang, Pen-Tzu ; Lee, Yi-Chen ; Wang, Yen-Yun ; Su, Yu-Han ; Hu, Stephen Chu-Sung ; Chen, Yuk-Kwan ; Tsui, Yu-Tong ; Kao, Ying-Hsien ; Huang, Ming-Yii ; Yuan, Shyng-Shiou F.</creatorcontrib><description>Background
Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear.
Patients and Methods
Eighty-seven patients with ESCC were enrolled in this study. Expression of Rad51 in ESCC was determined by immunohistochemistry and correlated with clinicopathological variables by Chi square test. The role of Rad51 in patient survival was determined by Kaplan–Meier estimates. The effects of Rad51 knockdown and overexpression on esophageal cancer growth, migration, and invasion were examined using TE8, CE81T, and KYSE70 cells. The mechanisms involved were also analyzed. Nude mice models were used for assessment of tumor growth.
Results
Rad51 staining was predominantly observed in ESCC patients. ESCC patients with high Rad51 expression had significantly decreased survival (
P
< 0.001) combined with increased tumor size (
P
= 0.034) and lymph node metastasis (
P
= 0.039). Rad51 overexpression promoted, while its knockdown attenuated, esophageal cancer cell viability through cell cycle entry and migration/invasion via epithelial–mesenchymal transition. Moreover, Rad51 overexpression increased colony formation in vitro and tumor growth in vivo. In addition, high Rad51 expression increased cancer progression through the p38/Akt/Snail signaling pathway.
Conclusions
This study indicates a new biological role for Rad51 in ESCC progression. Rad51 may serve as a potential prognostic biomarker and therapeutic target for ESCC patients.</description><identifier>ISSN: 1068-9265</identifier><identifier>EISSN: 1534-4681</identifier><identifier>DOI: 10.1245/s10434-019-08043-x</identifier><identifier>PMID: 31749080</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>AKT protein ; Animal models ; Animals ; Biomarkers, Tumor - analysis ; Cell cycle ; Cell migration ; Cell Movement ; Cell Proliferation ; Cell viability ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA Repair ; Double-strand break repair ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophageal Squamous Cell Carcinoma - genetics ; Esophageal Squamous Cell Carcinoma - pathology ; Esophagus ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Lymph nodes ; Lymphatic Metastasis - genetics ; Lymphatic Metastasis - pathology ; Male ; Medicine ; Medicine & Public Health ; Mesenchyme ; Metastases ; Metastasis ; Mice ; Mice, Nude ; Middle Aged ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Oncology ; Proto-Oncogene Proteins c-akt - metabolism ; Rad51 Recombinase - genetics ; Rad51 Recombinase - metabolism ; Signal Transduction ; Squamous cell carcinoma ; Surgery ; Surgical Oncology ; Telomeres ; Therapeutic applications ; Translational Research and Biomarkers</subject><ispartof>Annals of surgical oncology, 2020-06, Vol.27 (6), p.2090-2101</ispartof><rights>Society of Surgical Oncology 2019</rights><rights>Society of Surgical Oncology 2019.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-9da030a34bcf270741d1777fc83e79c22eef14ac91c08961aedde121db0a527a3</citedby><cites>FETCH-LOGICAL-c441t-9da030a34bcf270741d1777fc83e79c22eef14ac91c08961aedde121db0a527a3</cites><orcidid>0000-0002-4753-788X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1245/s10434-019-08043-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1245/s10434-019-08043-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31749080$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chiu, Wen-Chin</creatorcontrib><creatorcontrib>Fang, Pen-Tzu</creatorcontrib><creatorcontrib>Lee, Yi-Chen</creatorcontrib><creatorcontrib>Wang, Yen-Yun</creatorcontrib><creatorcontrib>Su, Yu-Han</creatorcontrib><creatorcontrib>Hu, Stephen Chu-Sung</creatorcontrib><creatorcontrib>Chen, Yuk-Kwan</creatorcontrib><creatorcontrib>Tsui, Yu-Tong</creatorcontrib><creatorcontrib>Kao, Ying-Hsien</creatorcontrib><creatorcontrib>Huang, Ming-Yii</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F.</creatorcontrib><title>DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway</title><title>Annals of surgical oncology</title><addtitle>Ann Surg Oncol</addtitle><addtitle>Ann Surg Oncol</addtitle><description>Background
Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear.
Patients and Methods
Eighty-seven patients with ESCC were enrolled in this study. Expression of Rad51 in ESCC was determined by immunohistochemistry and correlated with clinicopathological variables by Chi square test. The role of Rad51 in patient survival was determined by Kaplan–Meier estimates. The effects of Rad51 knockdown and overexpression on esophageal cancer growth, migration, and invasion were examined using TE8, CE81T, and KYSE70 cells. The mechanisms involved were also analyzed. Nude mice models were used for assessment of tumor growth.
Results
Rad51 staining was predominantly observed in ESCC patients. ESCC patients with high Rad51 expression had significantly decreased survival (
P
< 0.001) combined with increased tumor size (
P
= 0.034) and lymph node metastasis (
P
= 0.039). Rad51 overexpression promoted, while its knockdown attenuated, esophageal cancer cell viability through cell cycle entry and migration/invasion via epithelial–mesenchymal transition. Moreover, Rad51 overexpression increased colony formation in vitro and tumor growth in vivo. In addition, high Rad51 expression increased cancer progression through the p38/Akt/Snail signaling pathway.
Conclusions
This study indicates a new biological role for Rad51 in ESCC progression. Rad51 may serve as a potential prognostic biomarker and therapeutic target for ESCC patients.</description><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell viability</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Repair</subject><subject>Double-strand break repair</subject><subject>Esophageal cancer</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophageal Squamous Cell Carcinoma - genetics</subject><subject>Esophageal Squamous Cell Carcinoma - pathology</subject><subject>Esophagus</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis - genetics</subject><subject>Lymphatic Metastasis - pathology</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Oncology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rad51 Recombinase - genetics</subject><subject>Rad51 Recombinase - metabolism</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Surgery</subject><subject>Surgical Oncology</subject><subject>Telomeres</subject><subject>Therapeutic applications</subject><subject>Translational Research and Biomarkers</subject><issn>1068-9265</issn><issn>1534-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kE1P3DAQhi1EVT7aP8ChssQ5xWM76-S4WihFoi0CerZm7QkbuomDnRS48ssxLG1vlSx5ZD_vO9LD2AGIzyB1eZRAaKULAXUhqjwWD1tsF8r8pGcVbOdZzKqilrNyh-2ldCsEGCXK92xHgdF1zuyyp-Pvc35JA7aRX8QwUtvzS_Ql8LPeT44Sv566EPlpDPfjimPv-TcaMeXTJp7hkxSGFd4QrvnV3YRdmBJf0HrNFxhd24cO-e8WOfJBVUfzX2NxTAP1nvqRX-C4usfHD-xdg-tEH9_uffbzy8n14mtx_uP0bDE_L5zWMBa1R6EEKr10jTTCaPBgjGlcpcjUTkqiBjS6Gpyo6hkgeU8gwS8FltKg2meHm94hhruJ0mhvwxT7vNJKLYQojZGQKbmhXAwpRWrsENsO46MFYV-02412m7XbV-32IYc-vVVPy47838gfzxlQGyDlr_6G4r_d_6l9BqB_jbI</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Chiu, Wen-Chin</creator><creator>Fang, Pen-Tzu</creator><creator>Lee, Yi-Chen</creator><creator>Wang, Yen-Yun</creator><creator>Su, Yu-Han</creator><creator>Hu, Stephen Chu-Sung</creator><creator>Chen, Yuk-Kwan</creator><creator>Tsui, Yu-Tong</creator><creator>Kao, Ying-Hsien</creator><creator>Huang, Ming-Yii</creator><creator>Yuan, Shyng-Shiou F.</creator><general>Springer International Publishing</general><general>Springer Nature B.V</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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><orcidid>https://orcid.org/0000-0002-4753-788X</orcidid></search><sort><creationdate>20200601</creationdate><title>DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway</title><author>Chiu, Wen-Chin ; Fang, Pen-Tzu ; Lee, Yi-Chen ; Wang, Yen-Yun ; Su, Yu-Han ; Hu, Stephen Chu-Sung ; Chen, Yuk-Kwan ; Tsui, Yu-Tong ; Kao, Ying-Hsien ; Huang, Ming-Yii ; Yuan, Shyng-Shiou F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-9da030a34bcf270741d1777fc83e79c22eef14ac91c08961aedde121db0a527a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>AKT protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Cell cycle</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cell viability</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA Repair</topic><topic>Double-strand break repair</topic><topic>Esophageal cancer</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophageal Squamous Cell Carcinoma - genetics</topic><topic>Esophageal Squamous Cell Carcinoma - pathology</topic><topic>Esophagus</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis - genetics</topic><topic>Lymphatic Metastasis - pathology</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Oncology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rad51 Recombinase - genetics</topic><topic>Rad51 Recombinase - metabolism</topic><topic>Signal Transduction</topic><topic>Squamous cell carcinoma</topic><topic>Surgery</topic><topic>Surgical Oncology</topic><topic>Telomeres</topic><topic>Therapeutic applications</topic><topic>Translational Research and Biomarkers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chiu, Wen-Chin</creatorcontrib><creatorcontrib>Fang, Pen-Tzu</creatorcontrib><creatorcontrib>Lee, Yi-Chen</creatorcontrib><creatorcontrib>Wang, Yen-Yun</creatorcontrib><creatorcontrib>Su, Yu-Han</creatorcontrib><creatorcontrib>Hu, Stephen Chu-Sung</creatorcontrib><creatorcontrib>Chen, Yuk-Kwan</creatorcontrib><creatorcontrib>Tsui, Yu-Tong</creatorcontrib><creatorcontrib>Kao, Ying-Hsien</creatorcontrib><creatorcontrib>Huang, Ming-Yii</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</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>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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</collection><collection>ProQuest One Community College</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>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><jtitle>Annals of surgical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chiu, Wen-Chin</au><au>Fang, Pen-Tzu</au><au>Lee, Yi-Chen</au><au>Wang, Yen-Yun</au><au>Su, Yu-Han</au><au>Hu, Stephen Chu-Sung</au><au>Chen, Yuk-Kwan</au><au>Tsui, Yu-Tong</au><au>Kao, Ying-Hsien</au><au>Huang, Ming-Yii</au><au>Yuan, Shyng-Shiou F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway</atitle><jtitle>Annals of surgical oncology</jtitle><stitle>Ann Surg Oncol</stitle><addtitle>Ann Surg Oncol</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>27</volume><issue>6</issue><spage>2090</spage><epage>2101</epage><pages>2090-2101</pages><issn>1068-9265</issn><eissn>1534-4681</eissn><abstract>Background
Rad51 is a protein which plays a vital role in DNA double-strand break repair and maintenance of telomeres. However, the underlying mechanism for its action in esophageal squamous cell carcinoma (ESCC) remains unclear.
Patients and Methods
Eighty-seven patients with ESCC were enrolled in this study. Expression of Rad51 in ESCC was determined by immunohistochemistry and correlated with clinicopathological variables by Chi square test. The role of Rad51 in patient survival was determined by Kaplan–Meier estimates. The effects of Rad51 knockdown and overexpression on esophageal cancer growth, migration, and invasion were examined using TE8, CE81T, and KYSE70 cells. The mechanisms involved were also analyzed. Nude mice models were used for assessment of tumor growth.
Results
Rad51 staining was predominantly observed in ESCC patients. ESCC patients with high Rad51 expression had significantly decreased survival (
P
< 0.001) combined with increased tumor size (
P
= 0.034) and lymph node metastasis (
P
= 0.039). Rad51 overexpression promoted, while its knockdown attenuated, esophageal cancer cell viability through cell cycle entry and migration/invasion via epithelial–mesenchymal transition. Moreover, Rad51 overexpression increased colony formation in vitro and tumor growth in vivo. In addition, high Rad51 expression increased cancer progression through the p38/Akt/Snail signaling pathway.
Conclusions
This study indicates a new biological role for Rad51 in ESCC progression. Rad51 may serve as a potential prognostic biomarker and therapeutic target for ESCC patients.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>31749080</pmid><doi>10.1245/s10434-019-08043-x</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-4753-788X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1068-9265 |
| ispartof | Annals of surgical oncology, 2020-06, Vol.27 (6), p.2090-2101 |
| issn | 1068-9265 1534-4681 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | AKT protein Animal models Animals Biomarkers, Tumor - analysis Cell cycle Cell migration Cell Movement Cell Proliferation Cell viability Deoxyribonucleic acid DNA DNA damage DNA Repair Double-strand break repair Esophageal cancer Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Esophageal Squamous Cell Carcinoma - genetics Esophageal Squamous Cell Carcinoma - pathology Esophagus Female Gene Expression Regulation, Neoplastic Humans Immunohistochemistry Kaplan-Meier Estimate Lymph nodes Lymphatic Metastasis - genetics Lymphatic Metastasis - pathology Male Medicine Medicine & Public Health Mesenchyme Metastases Metastasis Mice Mice, Nude Middle Aged Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Oncology Proto-Oncogene Proteins c-akt - metabolism Rad51 Recombinase - genetics Rad51 Recombinase - metabolism Signal Transduction Squamous cell carcinoma Surgery Surgical Oncology Telomeres Therapeutic applications Translational Research and Biomarkers |
| title | DNA Repair Protein Rad51 Induces Tumor Growth and Metastasis in Esophageal Squamous Cell Carcinoma via a p38/Akt-Dependent Pathway |
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