Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer
Purpose DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known. Methods CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 ( n = 90). Tissue microarray con...
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| Veröffentlicht in: | Cellular oncology (Dordrecht) 2020-06, Vol.43 (3), p.409-420 |
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| creator | He, Jie Huang, Hongli Du, Yanlei Peng, Dong Zhou, Youlian Li, Yuyuan Wang, Hong Zhou, Yongjian Nie, Yuqiang |
| description | Purpose
DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known.
Methods
CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (
n
= 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines.
Results
DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (
p
|
| doi_str_mv | 10.1007/s13402-020-00495-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2377342903</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2377342903</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-f4737b016418d7e714af8e1f38e539dfb1b80373d16517e9ee0e49f9770c1eb13</originalsourceid><addsrcrecordid>eNp9kU1PwzAMhiMEYgj4AxxQJS5cCnaSNu1xjE9pEhc4hzZ1R6euGUkL4t8TKAyJA7kkdh6_cfwydoRwhgDq3KOQwGPgEAPIPImzLbbHOWIspEi3N2eeTdih90sIS6aYJukumwiOaZpkfI89Tb23pin6xnaRraPL2cX8kkfD2tFiaMf0W9M_R_2wsi5aO7tw5P1nuuiqaG1D0g_utXkt2qjpImNb68j0ITJFZ8gdsJ26aD0dfu_77PH66mF2G8_vb-5m03lshEr6uJZKqBIwlZhVihTKos4Ia5FRIvKqLrHMQChRhR-gopwISOZ1rhQYpBLFPjsddUOLLwP5Xq8ab6hti47s4DUXSoVp5CACevIHXdrBdaE7zSUgFwIgDxQfKeOs945qvXbNqnDvGkF_WqBHC3SwQH9ZoLNQdPwtPZQrqjYlPwMPgBgBH666Bbnft_-R_QA_gZBY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2401233009</pqid></control><display><type>article</type><title>Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>He, Jie ; Huang, Hongli ; Du, Yanlei ; Peng, Dong ; Zhou, Youlian ; Li, Yuyuan ; Wang, Hong ; Zhou, Yongjian ; Nie, Yuqiang</creator><creatorcontrib>He, Jie ; Huang, Hongli ; Du, Yanlei ; Peng, Dong ; Zhou, Youlian ; Li, Yuyuan ; Wang, Hong ; Zhou, Yongjian ; Nie, Yuqiang</creatorcontrib><description>Purpose
DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known.
Methods
CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (
n
= 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines.
Results
DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (
p
< 0.001). In addition, we found that DCBLD2 expression was positively correlated with the stage of the disease, the degree of differentiation and vascular invasion. High DCBLD2 expression was significantly associated with a poor overall survival. In vitro, DCBLD2 expression downregulation significantly reduced CRC cell proliferation and invasion. In a mouse xenograft model, DCBLD2 expression downregulation reduced lung metastasis and increased overall survival. Gene set enrichment analysis (GSEA) revealed that DCBLD2 overexpression induces epithelial–mesenchymal transition (EMT) and activates the JAK/STAT3 pathway.
Conclusions
We found that high DCBLD2 expression correlated with a poor clinical outcome, as well as tumorigenesis, invasion and metastasis of CRC cells. DCBLD2 may serve as a prognostic biomarker and a novel therapeutic target for CRC.</description><identifier>ISSN: 2211-3428</identifier><identifier>EISSN: 2211-3436</identifier><identifier>DOI: 10.1007/s13402-020-00495-8</identifier><identifier>PMID: 32166582</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aged ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Cancer Research ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Disease Progression ; DNA microarrays ; Down-Regulation - genetics ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Gene set enrichment analysis ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Male ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mesenchyme ; Metastases ; Metastasis ; Mice, Inbred BALB C ; Mice, Nude ; Middle Aged ; Neoplasm Metastasis ; Oncogenes ; Oncology ; Pathology ; Prognosis ; Signal Transduction ; Stat3 protein ; Surgery ; Survival Analysis ; Therapeutic applications ; Tumorigenesis ; Up-Regulation - genetics ; Xenografts</subject><ispartof>Cellular oncology (Dordrecht), 2020-06, Vol.43 (3), p.409-420</ispartof><rights>International Society for Cellular Oncology 2020</rights><rights>International Society for Cellular Oncology 2020.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-f4737b016418d7e714af8e1f38e539dfb1b80373d16517e9ee0e49f9770c1eb13</citedby><cites>FETCH-LOGICAL-c375t-f4737b016418d7e714af8e1f38e539dfb1b80373d16517e9ee0e49f9770c1eb13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s13402-020-00495-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13402-020-00495-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32166582$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Jie</creatorcontrib><creatorcontrib>Huang, Hongli</creatorcontrib><creatorcontrib>Du, Yanlei</creatorcontrib><creatorcontrib>Peng, Dong</creatorcontrib><creatorcontrib>Zhou, Youlian</creatorcontrib><creatorcontrib>Li, Yuyuan</creatorcontrib><creatorcontrib>Wang, Hong</creatorcontrib><creatorcontrib>Zhou, Yongjian</creatorcontrib><creatorcontrib>Nie, Yuqiang</creatorcontrib><title>Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer</title><title>Cellular oncology (Dordrecht)</title><addtitle>Cell Oncol</addtitle><addtitle>Cell Oncol (Dordr)</addtitle><description>Purpose
DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known.
Methods
CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (
n
= 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines.
Results
DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (
p
< 0.001). In addition, we found that DCBLD2 expression was positively correlated with the stage of the disease, the degree of differentiation and vascular invasion. High DCBLD2 expression was significantly associated with a poor overall survival. In vitro, DCBLD2 expression downregulation significantly reduced CRC cell proliferation and invasion. In a mouse xenograft model, DCBLD2 expression downregulation reduced lung metastasis and increased overall survival. Gene set enrichment analysis (GSEA) revealed that DCBLD2 overexpression induces epithelial–mesenchymal transition (EMT) and activates the JAK/STAT3 pathway.
Conclusions
We found that high DCBLD2 expression correlated with a poor clinical outcome, as well as tumorigenesis, invasion and metastasis of CRC cells. DCBLD2 may serve as a prognostic biomarker and a novel therapeutic target for CRC.</description><subject>Aged</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Disease Progression</subject><subject>DNA microarrays</subject><subject>Down-Regulation - genetics</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene set enrichment analysis</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Oncogenes</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Prognosis</subject><subject>Signal Transduction</subject><subject>Stat3 protein</subject><subject>Surgery</subject><subject>Survival Analysis</subject><subject>Therapeutic applications</subject><subject>Tumorigenesis</subject><subject>Up-Regulation - genetics</subject><subject>Xenografts</subject><issn>2211-3428</issn><issn>2211-3436</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1PwzAMhiMEYgj4AxxQJS5cCnaSNu1xjE9pEhc4hzZ1R6euGUkL4t8TKAyJA7kkdh6_cfwydoRwhgDq3KOQwGPgEAPIPImzLbbHOWIspEi3N2eeTdih90sIS6aYJukumwiOaZpkfI89Tb23pin6xnaRraPL2cX8kkfD2tFiaMf0W9M_R_2wsi5aO7tw5P1nuuiqaG1D0g_utXkt2qjpImNb68j0ITJFZ8gdsJ26aD0dfu_77PH66mF2G8_vb-5m03lshEr6uJZKqBIwlZhVihTKos4Ia5FRIvKqLrHMQChRhR-gopwISOZ1rhQYpBLFPjsddUOLLwP5Xq8ab6hti47s4DUXSoVp5CACevIHXdrBdaE7zSUgFwIgDxQfKeOs945qvXbNqnDvGkF_WqBHC3SwQH9ZoLNQdPwtPZQrqjYlPwMPgBgBH666Bbnft_-R_QA_gZBY</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>He, Jie</creator><creator>Huang, Hongli</creator><creator>Du, Yanlei</creator><creator>Peng, Dong</creator><creator>Zhou, Youlian</creator><creator>Li, Yuyuan</creator><creator>Wang, Hong</creator><creator>Zhou, Yongjian</creator><creator>Nie, Yuqiang</creator><general>Springer Netherlands</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>7X8</scope></search><sort><creationdate>20200601</creationdate><title>Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer</title><author>He, Jie ; Huang, Hongli ; Du, Yanlei ; Peng, Dong ; Zhou, Youlian ; Li, Yuyuan ; Wang, Hong ; Zhou, Yongjian ; Nie, Yuqiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-f4737b016418d7e714af8e1f38e539dfb1b80373d16517e9ee0e49f9770c1eb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Disease Progression</topic><topic>DNA microarrays</topic><topic>Down-Regulation - genetics</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene set enrichment analysis</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Oncogenes</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Prognosis</topic><topic>Signal Transduction</topic><topic>Stat3 protein</topic><topic>Surgery</topic><topic>Survival Analysis</topic><topic>Therapeutic applications</topic><topic>Tumorigenesis</topic><topic>Up-Regulation - genetics</topic><topic>Xenografts</topic><toplevel>online_resources</toplevel><creatorcontrib>He, Jie</creatorcontrib><creatorcontrib>Huang, Hongli</creatorcontrib><creatorcontrib>Du, Yanlei</creatorcontrib><creatorcontrib>Peng, Dong</creatorcontrib><creatorcontrib>Zhou, Youlian</creatorcontrib><creatorcontrib>Li, Yuyuan</creatorcontrib><creatorcontrib>Wang, Hong</creatorcontrib><creatorcontrib>Zhou, Yongjian</creatorcontrib><creatorcontrib>Nie, Yuqiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular oncology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Jie</au><au>Huang, Hongli</au><au>Du, Yanlei</au><au>Peng, Dong</au><au>Zhou, Youlian</au><au>Li, Yuyuan</au><au>Wang, Hong</au><au>Zhou, Yongjian</au><au>Nie, Yuqiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer</atitle><jtitle>Cellular oncology (Dordrecht)</jtitle><stitle>Cell Oncol</stitle><addtitle>Cell Oncol (Dordr)</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>43</volume><issue>3</issue><spage>409</spage><epage>420</epage><pages>409-420</pages><issn>2211-3428</issn><eissn>2211-3436</eissn><abstract>Purpose
DCBLD2 expression dysregulation has been reported in several types of human cancer. As yet, however, the role of DCBLD2 in colorectal cancer (CRC) is not known.
Methods
CRC tissues were obtained from patients undergoing surgery from February 2009 to May 2014 (
n
= 90). Tissue microarray construction and immunohistochemistry were carried out to determine DCBLD2 expression. In vivo studies were performed in 4-week-old BALB/c nude mice. In vitro studies were conducted using CRC-derived HT29 and HCT116 cell lines.
Results
DCBLD2 expression was found to be significantly increased in CRC tissues compared to adjacent normal tissues (
p
< 0.001). In addition, we found that DCBLD2 expression was positively correlated with the stage of the disease, the degree of differentiation and vascular invasion. High DCBLD2 expression was significantly associated with a poor overall survival. In vitro, DCBLD2 expression downregulation significantly reduced CRC cell proliferation and invasion. In a mouse xenograft model, DCBLD2 expression downregulation reduced lung metastasis and increased overall survival. Gene set enrichment analysis (GSEA) revealed that DCBLD2 overexpression induces epithelial–mesenchymal transition (EMT) and activates the JAK/STAT3 pathway.
Conclusions
We found that high DCBLD2 expression correlated with a poor clinical outcome, as well as tumorigenesis, invasion and metastasis of CRC cells. DCBLD2 may serve as a prognostic biomarker and a novel therapeutic target for CRC.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>32166582</pmid><doi>10.1007/s13402-020-00495-8</doi><tpages>12</tpages></addata></record> |
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| subjects | Aged Animals Biomedical and Life Sciences Biomedicine Cancer Cancer Research Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Disease Progression DNA microarrays Down-Regulation - genetics Epithelial-Mesenchymal Transition - genetics Female Gene Expression Regulation, Neoplastic Gene set enrichment analysis Humans Immunohistochemistry Kaplan-Meier Estimate Male Membrane Proteins - genetics Membrane Proteins - metabolism Mesenchyme Metastases Metastasis Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Metastasis Oncogenes Oncology Pathology Prognosis Signal Transduction Stat3 protein Surgery Survival Analysis Therapeutic applications Tumorigenesis Up-Regulation - genetics Xenografts |
| title | Association of DCBLD2 upregulation with tumor progression and poor survival in colorectal cancer |
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