B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration
Background B7 homolog 3 (B7-H3), a member of the immunoregulatory ligand B7 family, is pivotal in T-cell-mediated immune response. It is widely expressed in diverse human tumors and its high expression indicates the poor prognosis of the patients. Nonetheless, B7-H3’s role in colorectal cancer (CRC)...
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| Veröffentlicht in: | Cell biochemistry and biophysics 2021-06, Vol.79 (2), p.397-405 |
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| creator | Hu, Xiaomao Xu, Minxian Hu, Yangzhi Li, Na Zhou, Lei |
| description | Background
B7 homolog 3 (B7-H3), a member of the immunoregulatory ligand B7 family, is pivotal in T-cell-mediated immune response. It is widely expressed in diverse human tumors and its high expression indicates the poor prognosis of the patients. Nonetheless, B7-H3’s role in colorectal cancer (CRC) needs to be further explored.
Methods
Western blot and immunohistochemistry were employed for detecting B7-H3 protein expression in CRC tissues and cell lines, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting B7-H3 mRNA and miR-128 expression levels. CRC cell lines SW620 and HT29 were used to construct B7-H3 overexpression or knockdown cell models, respectively. Cell counting kit-8 (CCK-8), 5-bromo-2′-deoxyuridine (BrdU), and scratch wound healing assays were employed for evaluating the effects of B7-H3 on CRC cell multiplication and migration. Besides, the regulatory relationship between miR-128 and B7-H3 was validated through dual-luciferase reporter gene assay, qRT-PCR, and western blotting.
Results
B7-H3 expression level was remarkably elevated in CRC tissues and cell lines, and its high expression level was associated with increased tumor size, positive lymph node metastasis, and increased T stage. In CRC cells, B7-H3 overexpression significantly facilitated the cell multiplication and migration, while B7-H3 knockdown worked oppositely. Moreover, B7-H3 was identified as a target of miR-128, and miR-128 negatively regulated B7-H3 expression in CRC cells.
Conclusion
B7-H3 expression is upregulated in CRC tissues and cell lines, and B7-H3 participates in promoting the proliferation and migration of CRC cells. Besides, B7-H3 expression is negatively regulated by miR-128 in CRC. |
| doi_str_mv | 10.1007/s12013-021-00975-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2503435125</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2503435125</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-afe350fd75e2b7f36f217eec23168768de4400faab29b415bb34eedb5806721d3</originalsourceid><addsrcrecordid>eNp9kUtv1TAQhS1ERUvhD7BAltiwqNsZP66TZYmAVuoDVbC2nGRylSqJWztBuv--LikgddGV7TnfnBn5MPYB4RgB7ElCCagESBQApTUCXrEDNKbMpUK9zncojCixNPvsbUq3AFKC1m_YvlJWK9TygDVfrDhTR_yKtn7uf9Ow4ze0XQY_U8vrHR_7G4GyOOI_YhjDTIlXYQiRmtkPvPJTQ5FXNAyP-tB3FLNLmLifWn7Zb9fXO7bX-SHR-6fzkP369vVndSYurr-fV6cXolHWzMJ3pAx0rTUka9upTSfREjVS4aawm6IlrQE672tZ1hpNXStN1NamgI2V2KpD9nn1vYvhfqE0u7FPTV7OTxSW5KQBpZVBaTL66Rl6G5Y45e0yJbWxiLbMlFypJoaUInXuLvajjzuH4B4jcGsELkfg_kTgIDd9fLJe6pHafy1__zwDagVSlqYtxf-zX7B9ADEQjxw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2524571179</pqid></control><display><type>article</type><title>B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Hu, Xiaomao ; Xu, Minxian ; Hu, Yangzhi ; Li, Na ; Zhou, Lei</creator><creatorcontrib>Hu, Xiaomao ; Xu, Minxian ; Hu, Yangzhi ; Li, Na ; Zhou, Lei</creatorcontrib><description>Background
B7 homolog 3 (B7-H3), a member of the immunoregulatory ligand B7 family, is pivotal in T-cell-mediated immune response. It is widely expressed in diverse human tumors and its high expression indicates the poor prognosis of the patients. Nonetheless, B7-H3’s role in colorectal cancer (CRC) needs to be further explored.
Methods
Western blot and immunohistochemistry were employed for detecting B7-H3 protein expression in CRC tissues and cell lines, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting B7-H3 mRNA and miR-128 expression levels. CRC cell lines SW620 and HT29 were used to construct B7-H3 overexpression or knockdown cell models, respectively. Cell counting kit-8 (CCK-8), 5-bromo-2′-deoxyuridine (BrdU), and scratch wound healing assays were employed for evaluating the effects of B7-H3 on CRC cell multiplication and migration. Besides, the regulatory relationship between miR-128 and B7-H3 was validated through dual-luciferase reporter gene assay, qRT-PCR, and western blotting.
Results
B7-H3 expression level was remarkably elevated in CRC tissues and cell lines, and its high expression level was associated with increased tumor size, positive lymph node metastasis, and increased T stage. In CRC cells, B7-H3 overexpression significantly facilitated the cell multiplication and migration, while B7-H3 knockdown worked oppositely. Moreover, B7-H3 was identified as a target of miR-128, and miR-128 negatively regulated B7-H3 expression in CRC cells.
Conclusion
B7-H3 expression is upregulated in CRC tissues and cell lines, and B7-H3 participates in promoting the proliferation and migration of CRC cells. Besides, B7-H3 expression is negatively regulated by miR-128 in CRC.</description><identifier>ISSN: 1085-9195</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-021-00975-0</identifier><identifier>PMID: 33743142</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antagomirs - metabolism ; B7 antigen ; B7 Antigens - antagonists & inhibitors ; B7 Antigens - genetics ; B7 Antigens - metabolism ; Base Sequence ; Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Cancer ; Cell Biology ; Cell culture ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cholecystokinin ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - mortality ; Colorectal Neoplasms - pathology ; Female ; Gene expression ; Homology ; Humans ; Immune response ; Immune response (cell-mediated) ; Immune system ; Immunohistochemistry ; Immunoregulation ; Life Sciences ; Lymph nodes ; Lymphocytes T ; Male ; Metastases ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; mRNA ; Multiplication ; Neoplasm Staging ; Original Paper ; Pharmacology/Toxicology ; Polymerase chain reaction ; Reporter gene ; RNA Interference ; RNA, Small Interfering - metabolism ; Sequence Alignment ; Survival Rate ; Target recognition ; Tumors ; Western blotting ; Wound healing</subject><ispartof>Cell biochemistry and biophysics, 2021-06, Vol.79 (2), p.397-405</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-afe350fd75e2b7f36f217eec23168768de4400faab29b415bb34eedb5806721d3</citedby><cites>FETCH-LOGICAL-c375t-afe350fd75e2b7f36f217eec23168768de4400faab29b415bb34eedb5806721d3</cites><orcidid>0000-0002-8094-3441</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12013-021-00975-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-021-00975-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33743142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Xiaomao</creatorcontrib><creatorcontrib>Xu, Minxian</creatorcontrib><creatorcontrib>Hu, Yangzhi</creatorcontrib><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Zhou, Lei</creatorcontrib><title>B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><addtitle>Cell Biochem Biophys</addtitle><description>Background
B7 homolog 3 (B7-H3), a member of the immunoregulatory ligand B7 family, is pivotal in T-cell-mediated immune response. It is widely expressed in diverse human tumors and its high expression indicates the poor prognosis of the patients. Nonetheless, B7-H3’s role in colorectal cancer (CRC) needs to be further explored.
Methods
Western blot and immunohistochemistry were employed for detecting B7-H3 protein expression in CRC tissues and cell lines, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting B7-H3 mRNA and miR-128 expression levels. CRC cell lines SW620 and HT29 were used to construct B7-H3 overexpression or knockdown cell models, respectively. Cell counting kit-8 (CCK-8), 5-bromo-2′-deoxyuridine (BrdU), and scratch wound healing assays were employed for evaluating the effects of B7-H3 on CRC cell multiplication and migration. Besides, the regulatory relationship between miR-128 and B7-H3 was validated through dual-luciferase reporter gene assay, qRT-PCR, and western blotting.
Results
B7-H3 expression level was remarkably elevated in CRC tissues and cell lines, and its high expression level was associated with increased tumor size, positive lymph node metastasis, and increased T stage. In CRC cells, B7-H3 overexpression significantly facilitated the cell multiplication and migration, while B7-H3 knockdown worked oppositely. Moreover, B7-H3 was identified as a target of miR-128, and miR-128 negatively regulated B7-H3 expression in CRC cells.
Conclusion
B7-H3 expression is upregulated in CRC tissues and cell lines, and B7-H3 participates in promoting the proliferation and migration of CRC cells. Besides, B7-H3 expression is negatively regulated by miR-128 in CRC.</description><subject>Antagomirs - metabolism</subject><subject>B7 antigen</subject><subject>B7 Antigens - antagonists & inhibitors</subject><subject>B7 Antigens - genetics</subject><subject>B7 Antigens - metabolism</subject><subject>Base Sequence</subject><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cholecystokinin</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - mortality</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Female</subject><subject>Gene expression</subject><subject>Homology</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune response (cell-mediated)</subject><subject>Immune system</subject><subject>Immunohistochemistry</subject><subject>Immunoregulation</subject><subject>Life Sciences</subject><subject>Lymph nodes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Metastases</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>mRNA</subject><subject>Multiplication</subject><subject>Neoplasm Staging</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Polymerase chain reaction</subject><subject>Reporter gene</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Sequence Alignment</subject><subject>Survival Rate</subject><subject>Target recognition</subject><subject>Tumors</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>1085-9195</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</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><sourceid>GNUQQ</sourceid><recordid>eNp9kUtv1TAQhS1ERUvhD7BAltiwqNsZP66TZYmAVuoDVbC2nGRylSqJWztBuv--LikgddGV7TnfnBn5MPYB4RgB7ElCCagESBQApTUCXrEDNKbMpUK9zncojCixNPvsbUq3AFKC1m_YvlJWK9TygDVfrDhTR_yKtn7uf9Ow4ze0XQY_U8vrHR_7G4GyOOI_YhjDTIlXYQiRmtkPvPJTQ5FXNAyP-tB3FLNLmLifWn7Zb9fXO7bX-SHR-6fzkP369vVndSYurr-fV6cXolHWzMJ3pAx0rTUka9upTSfREjVS4aawm6IlrQE672tZ1hpNXStN1NamgI2V2KpD9nn1vYvhfqE0u7FPTV7OTxSW5KQBpZVBaTL66Rl6G5Y45e0yJbWxiLbMlFypJoaUInXuLvajjzuH4B4jcGsELkfg_kTgIDd9fLJe6pHafy1__zwDagVSlqYtxf-zX7B9ADEQjxw</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Hu, Xiaomao</creator><creator>Xu, Minxian</creator><creator>Hu, Yangzhi</creator><creator>Li, Na</creator><creator>Zhou, Lei</creator><general>Springer US</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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8094-3441</orcidid></search><sort><creationdate>20210601</creationdate><title>B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration</title><author>Hu, Xiaomao ; Xu, Minxian ; Hu, Yangzhi ; Li, Na ; Zhou, Lei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-afe350fd75e2b7f36f217eec23168768de4400faab29b415bb34eedb5806721d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Antagomirs - metabolism</topic><topic>B7 antigen</topic><topic>B7 Antigens - antagonists & inhibitors</topic><topic>B7 Antigens - genetics</topic><topic>B7 Antigens - metabolism</topic><topic>Base Sequence</topic><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biophysics</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cholecystokinin</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - mortality</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Female</topic><topic>Gene expression</topic><topic>Homology</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune response (cell-mediated)</topic><topic>Immune system</topic><topic>Immunohistochemistry</topic><topic>Immunoregulation</topic><topic>Life Sciences</topic><topic>Lymph nodes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Metastases</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>mRNA</topic><topic>Multiplication</topic><topic>Neoplasm Staging</topic><topic>Original Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Polymerase chain reaction</topic><topic>Reporter gene</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Sequence Alignment</topic><topic>Survival Rate</topic><topic>Target recognition</topic><topic>Tumors</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Xiaomao</creatorcontrib><creatorcontrib>Xu, Minxian</creatorcontrib><creatorcontrib>Hu, Yangzhi</creatorcontrib><creatorcontrib>Li, Na</creatorcontrib><creatorcontrib>Zhou, Lei</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Xiaomao</au><au>Xu, Minxian</au><au>Hu, Yangzhi</au><au>Li, Na</au><au>Zhou, Lei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><addtitle>Cell Biochem Biophys</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>79</volume><issue>2</issue><spage>397</spage><epage>405</epage><pages>397-405</pages><issn>1085-9195</issn><eissn>1559-0283</eissn><abstract>Background
B7 homolog 3 (B7-H3), a member of the immunoregulatory ligand B7 family, is pivotal in T-cell-mediated immune response. It is widely expressed in diverse human tumors and its high expression indicates the poor prognosis of the patients. Nonetheless, B7-H3’s role in colorectal cancer (CRC) needs to be further explored.
Methods
Western blot and immunohistochemistry were employed for detecting B7-H3 protein expression in CRC tissues and cell lines, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting B7-H3 mRNA and miR-128 expression levels. CRC cell lines SW620 and HT29 were used to construct B7-H3 overexpression or knockdown cell models, respectively. Cell counting kit-8 (CCK-8), 5-bromo-2′-deoxyuridine (BrdU), and scratch wound healing assays were employed for evaluating the effects of B7-H3 on CRC cell multiplication and migration. Besides, the regulatory relationship between miR-128 and B7-H3 was validated through dual-luciferase reporter gene assay, qRT-PCR, and western blotting.
Results
B7-H3 expression level was remarkably elevated in CRC tissues and cell lines, and its high expression level was associated with increased tumor size, positive lymph node metastasis, and increased T stage. In CRC cells, B7-H3 overexpression significantly facilitated the cell multiplication and migration, while B7-H3 knockdown worked oppositely. Moreover, B7-H3 was identified as a target of miR-128, and miR-128 negatively regulated B7-H3 expression in CRC cells.
Conclusion
B7-H3 expression is upregulated in CRC tissues and cell lines, and B7-H3 participates in promoting the proliferation and migration of CRC cells. Besides, B7-H3 expression is negatively regulated by miR-128 in CRC.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33743142</pmid><doi>10.1007/s12013-021-00975-0</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8094-3441</orcidid></addata></record> |
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| subjects | Antagomirs - metabolism B7 antigen B7 Antigens - antagonists & inhibitors B7 Antigens - genetics B7 Antigens - metabolism Base Sequence Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Cancer Cell Biology Cell culture Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cholecystokinin Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - metabolism Colorectal Neoplasms - mortality Colorectal Neoplasms - pathology Female Gene expression Homology Humans Immune response Immune response (cell-mediated) Immune system Immunohistochemistry Immunoregulation Life Sciences Lymph nodes Lymphocytes T Male Metastases MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism Middle Aged mRNA Multiplication Neoplasm Staging Original Paper Pharmacology/Toxicology Polymerase chain reaction Reporter gene RNA Interference RNA, Small Interfering - metabolism Sequence Alignment Survival Rate Target recognition Tumors Western blotting Wound healing |
| title | B7-H3, Negatively Regulated by miR-128, Promotes Colorectal Cancer Cell Proliferation and Migration |
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