Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer
Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very‐low‐density‐lipoprotein receptor (VLDLR), a member of the low‐density‐lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by b...
Gespeichert in:
Veröffentlicht in: | Molecular carcinogenesis 2017-06, Vol.56 (6), p.1620-1629 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 1629 |
---|---|
container_issue | 6 |
container_start_page | 1620 |
container_title | Molecular carcinogenesis |
container_volume | 56 |
creator | Kim, Bong‐Kyu Yoo, Hye‐In Lee, Ah‐Reum Choi, Keonwoo Yoon, Sungjoo Kim |
description | Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very‐low‐density‐lipoprotein receptor (VLDLR), a member of the low‐density‐lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by binding numerous ligands. Several studies reported the altered expression of VLDLR and suggested that VLDLR may play a critical role in tumor development by affecting cell proliferation and metastasis. However, the function of VLDLR and regulation of its expression by miRNAs have not been investigated in CRC. In the present study, we investigated the expression of VLDLR in CRC patients and found it to be significantly decreased in tumors in comparison with paired adjacent non‐tumor tissues. Moreover, VLDLR over‐expression inhibited the proliferation and migration of CRC cells. We also found that VLDLR expression was negatively regulated by miR‐200c in CRC cells and that their expression levels were inversely correlated in CRC patients. These data suggest that VLDLR down‐regulation mediated by the increased expression of miR‐200c may be involved in the development of CRC. |
doi_str_mv | 10.1002/mc.22618 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1861597228</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1896303654</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3498-7129813ab2e8804c0b64cf87a1bddb097f8dd811137beddd6efced203ba68f43</originalsourceid><addsrcrecordid>eNp10N9KwzAUx_EgiptT8Akk4I03nUnatemlbP6DijCGtzFNTllH2s6kde7OR_AZfRKjmyKCV-fmw5cfB6FjSoaUEHZeqSFjMeU7qE9JygOWRNEu6hOepgFNedJDB84tCKE0GZF91GOcUhZFYR89TkBZkA40hpelBefKpsZNgR-ySTbFpcNl_QzWgVlj1VgLRrbersp2jqty-v76xghRHuF5V8naG9NYUK00WMlagT1Ee4U0Do62d4BmV5ez8U2Q3V_fji-yQIWRX5xQlnIaypwB5yRSJI8jVfBE0lzrnKRJwbX2q2mY5KC1jqFQoBkJcxnzIgoH6GyTXdrmqQPXiqp0CoyRNTSdE5THdJQmjHFPT__QRdPZ2o_zKo1DEsajX0FlG-csFGJpy0rataBEfD5dVEp8Pd3Tk22wyyvQP_D7yx4EG7AqDaz_DYm78Sb4AUubinU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1896303654</pqid></control><display><type>article</type><title>Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer</title><source>MEDLINE</source><source>Wiley Online Library</source><creator>Kim, Bong‐Kyu ; Yoo, Hye‐In ; Lee, Ah‐Reum ; Choi, Keonwoo ; Yoon, Sungjoo Kim</creator><creatorcontrib>Kim, Bong‐Kyu ; Yoo, Hye‐In ; Lee, Ah‐Reum ; Choi, Keonwoo ; Yoon, Sungjoo Kim</creatorcontrib><description>Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very‐low‐density‐lipoprotein receptor (VLDLR), a member of the low‐density‐lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by binding numerous ligands. Several studies reported the altered expression of VLDLR and suggested that VLDLR may play a critical role in tumor development by affecting cell proliferation and metastasis. However, the function of VLDLR and regulation of its expression by miRNAs have not been investigated in CRC. In the present study, we investigated the expression of VLDLR in CRC patients and found it to be significantly decreased in tumors in comparison with paired adjacent non‐tumor tissues. Moreover, VLDLR over‐expression inhibited the proliferation and migration of CRC cells. We also found that VLDLR expression was negatively regulated by miR‐200c in CRC cells and that their expression levels were inversely correlated in CRC patients. These data suggest that VLDLR down‐regulation mediated by the increased expression of miR‐200c may be involved in the development of CRC.</description><identifier>ISSN: 0899-1987</identifier><identifier>EISSN: 1098-2744</identifier><identifier>DOI: 10.1002/mc.22618</identifier><identifier>PMID: 28112443</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Cell adhesion & migration ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Colon - metabolism ; Colon - pathology ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Down-Regulation ; Gene expression ; Gene Expression Regulation, Neoplastic ; Humans ; Low density lipoprotein receptors ; Metastases ; MicroRNAs - genetics ; miRNA ; miR‐200c ; Morbidity ; Overexpression ; Receptor density ; Receptors, LDL - genetics ; Rectum - metabolism ; Rectum - pathology ; Tissues ; Tumors ; VLDLR</subject><ispartof>Molecular carcinogenesis, 2017-06, Vol.56 (6), p.1620-1629</ispartof><rights>2017 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3498-7129813ab2e8804c0b64cf87a1bddb097f8dd811137beddd6efced203ba68f43</citedby><cites>FETCH-LOGICAL-c3498-7129813ab2e8804c0b64cf87a1bddb097f8dd811137beddd6efced203ba68f43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmc.22618$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmc.22618$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28112443$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Bong‐Kyu</creatorcontrib><creatorcontrib>Yoo, Hye‐In</creatorcontrib><creatorcontrib>Lee, Ah‐Reum</creatorcontrib><creatorcontrib>Choi, Keonwoo</creatorcontrib><creatorcontrib>Yoon, Sungjoo Kim</creatorcontrib><title>Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer</title><title>Molecular carcinogenesis</title><addtitle>Mol Carcinog</addtitle><description>Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very‐low‐density‐lipoprotein receptor (VLDLR), a member of the low‐density‐lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by binding numerous ligands. Several studies reported the altered expression of VLDLR and suggested that VLDLR may play a critical role in tumor development by affecting cell proliferation and metastasis. However, the function of VLDLR and regulation of its expression by miRNAs have not been investigated in CRC. In the present study, we investigated the expression of VLDLR in CRC patients and found it to be significantly decreased in tumors in comparison with paired adjacent non‐tumor tissues. Moreover, VLDLR over‐expression inhibited the proliferation and migration of CRC cells. We also found that VLDLR expression was negatively regulated by miR‐200c in CRC cells and that their expression levels were inversely correlated in CRC patients. These data suggest that VLDLR down‐regulation mediated by the increased expression of miR‐200c may be involved in the development of CRC.</description><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Colon - metabolism</subject><subject>Colon - pathology</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Down-Regulation</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Low density lipoprotein receptors</subject><subject>Metastases</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>miR‐200c</subject><subject>Morbidity</subject><subject>Overexpression</subject><subject>Receptor density</subject><subject>Receptors, LDL - genetics</subject><subject>Rectum - metabolism</subject><subject>Rectum - pathology</subject><subject>Tissues</subject><subject>Tumors</subject><subject>VLDLR</subject><issn>0899-1987</issn><issn>1098-2744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10N9KwzAUx_EgiptT8Akk4I03nUnatemlbP6DijCGtzFNTllH2s6kde7OR_AZfRKjmyKCV-fmw5cfB6FjSoaUEHZeqSFjMeU7qE9JygOWRNEu6hOepgFNedJDB84tCKE0GZF91GOcUhZFYR89TkBZkA40hpelBefKpsZNgR-ySTbFpcNl_QzWgVlj1VgLRrbersp2jqty-v76xghRHuF5V8naG9NYUK00WMlagT1Ee4U0Do62d4BmV5ez8U2Q3V_fji-yQIWRX5xQlnIaypwB5yRSJI8jVfBE0lzrnKRJwbX2q2mY5KC1jqFQoBkJcxnzIgoH6GyTXdrmqQPXiqp0CoyRNTSdE5THdJQmjHFPT__QRdPZ2o_zKo1DEsajX0FlG-csFGJpy0rataBEfD5dVEp8Pd3Tk22wyyvQP_D7yx4EG7AqDaz_DYm78Sb4AUubinU</recordid><startdate>201706</startdate><enddate>201706</enddate><creator>Kim, Bong‐Kyu</creator><creator>Yoo, Hye‐In</creator><creator>Lee, Ah‐Reum</creator><creator>Choi, Keonwoo</creator><creator>Yoon, Sungjoo Kim</creator><general>Wiley Subscription Services, Inc</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>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201706</creationdate><title>Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer</title><author>Kim, Bong‐Kyu ; Yoo, Hye‐In ; Lee, Ah‐Reum ; Choi, Keonwoo ; Yoon, Sungjoo Kim</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3498-7129813ab2e8804c0b64cf87a1bddb097f8dd811137beddd6efced203ba68f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Cell adhesion & migration</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Colon - metabolism</topic><topic>Colon - pathology</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Down-Regulation</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Low density lipoprotein receptors</topic><topic>Metastases</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>miR‐200c</topic><topic>Morbidity</topic><topic>Overexpression</topic><topic>Receptor density</topic><topic>Receptors, LDL - genetics</topic><topic>Rectum - metabolism</topic><topic>Rectum - pathology</topic><topic>Tissues</topic><topic>Tumors</topic><topic>VLDLR</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Bong‐Kyu</creatorcontrib><creatorcontrib>Yoo, Hye‐In</creatorcontrib><creatorcontrib>Lee, Ah‐Reum</creatorcontrib><creatorcontrib>Choi, Keonwoo</creatorcontrib><creatorcontrib>Yoon, Sungjoo Kim</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular carcinogenesis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Bong‐Kyu</au><au>Yoo, Hye‐In</au><au>Lee, Ah‐Reum</au><au>Choi, Keonwoo</au><au>Yoon, Sungjoo Kim</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer</atitle><jtitle>Molecular carcinogenesis</jtitle><addtitle>Mol Carcinog</addtitle><date>2017-06</date><risdate>2017</risdate><volume>56</volume><issue>6</issue><spage>1620</spage><epage>1629</epage><pages>1620-1629</pages><issn>0899-1987</issn><eissn>1098-2744</eissn><abstract>Colorectal cancer (CRC) is one of the most common cancers and has a high rate of morbidity and mortality worldwide. Very‐low‐density‐lipoprotein receptor (VLDLR), a member of the low‐density‐lipoprotein receptor (LDLR) superfamily, is a multifunctional receptor that regulates cellular signaling by binding numerous ligands. Several studies reported the altered expression of VLDLR and suggested that VLDLR may play a critical role in tumor development by affecting cell proliferation and metastasis. However, the function of VLDLR and regulation of its expression by miRNAs have not been investigated in CRC. In the present study, we investigated the expression of VLDLR in CRC patients and found it to be significantly decreased in tumors in comparison with paired adjacent non‐tumor tissues. Moreover, VLDLR over‐expression inhibited the proliferation and migration of CRC cells. We also found that VLDLR expression was negatively regulated by miR‐200c in CRC cells and that their expression levels were inversely correlated in CRC patients. These data suggest that VLDLR down‐regulation mediated by the increased expression of miR‐200c may be involved in the development of CRC.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28112443</pmid><doi>10.1002/mc.22618</doi><tpages>10</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0899-1987 |
ispartof | Molecular carcinogenesis, 2017-06, Vol.56 (6), p.1620-1629 |
issn | 0899-1987 1098-2744 |
language | eng |
recordid | cdi_proquest_miscellaneous_1861597228 |
source | MEDLINE; Wiley Online Library |
subjects | Cell adhesion & migration Cell Line, Tumor Cell Movement Cell Proliferation Colon - metabolism Colon - pathology Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Down-Regulation Gene expression Gene Expression Regulation, Neoplastic Humans Low density lipoprotein receptors Metastases MicroRNAs - genetics miRNA miR‐200c Morbidity Overexpression Receptor density Receptors, LDL - genetics Rectum - metabolism Rectum - pathology Tissues Tumors VLDLR |
title | Decreased expression of VLDLR is inversely correlated with miR‐200c in human colorectal cancer |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T15%3A23%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Decreased%20expression%20of%20VLDLR%20is%20inversely%20correlated%20with%20miR%E2%80%90200c%20in%20human%20colorectal%20cancer&rft.jtitle=Molecular%20carcinogenesis&rft.au=Kim,%20Bong%E2%80%90Kyu&rft.date=2017-06&rft.volume=56&rft.issue=6&rft.spage=1620&rft.epage=1629&rft.pages=1620-1629&rft.issn=0899-1987&rft.eissn=1098-2744&rft_id=info:doi/10.1002/mc.22618&rft_dat=%3Cproquest_cross%3E1896303654%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1896303654&rft_id=info:pmid/28112443&rfr_iscdi=true |