association of the expression of miR-122-5p and its target ADAM10 with human breast cancer
MicroRNAs can regulate many biological functions. miR-122-5p has a tumor suppressor function through different molecular pathways. Also, our second hit, ADAM10, targeted by miR-122-5p, is a major determinant of HER2 shedding causing that trastuzumab cannot bind to HER2 receptors. Therefore, our anal...
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| Veröffentlicht in: | Molecular biology reports 2015-02, Vol.42 (2), p.497-505 |
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| creator | Ergün, Sercan Ulasli, Mustafa Igci, Yusuf Ziya Igci, Mehri Kırkbes, Sevil Borazan, Ersin Balik, Ahmet Yumrutaş, Önder Camci, Celalettin Cakmak, Ecir Ali Arslan, Ahmet Oztuzcu, Serdar |
| description | MicroRNAs can regulate many biological functions. miR-122-5p has a tumor suppressor function through different molecular pathways. Also, our second hit, ADAM10, targeted by miR-122-5p, is a major determinant of HER2 shedding causing that trastuzumab cannot bind to HER2 receptors. Therefore, our analysis upon ADAM10 expression and miR-122-5p was a good point to understand molecular mechanism of breast cancer. In our study, we investigated the expression profiles of miR-122-5p and its target ADAM10 in 71 breast cancer patients. Immunohistochemical analysis of ER, PR and HER2 gene products was used to categorize tumors in patients. Expression data and immunohistochemical findings were evaluated to comment on the relationship between miR-122-5p and ADAM10. ADAM10 expression was higher in tumor than that of normal tissue but miR-122-5p expression was lower in tumor than that of normal tissue. The expression pattern in HER2+ patients was reverse of the overall result. It can be explained like that miR-122-5p expression increases especially in HER2+ cancer cell to suppress ADAM10 shedding activity on HER2 receptor. However, increase in expression of tumor suppressor miR-122-5p is not enough to inhibit ADAM10. All in all, we can think miR-122-5p as potential regulator of ADAM10 and trastuzumab resistance. Since if we increase miR-122-5p activity together with trastuzumab administration, then HER2+ breast cancer cells may overcome trastuzumab resistance by inhibiting ADAM10 shedding activity on HER2 receptors and increase the efficiency of trastuzumab. |
| doi_str_mv | 10.1007/s11033-014-3793-2 |
| format | Article |
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Also, our second hit, ADAM10, targeted by miR-122-5p, is a major determinant of HER2 shedding causing that trastuzumab cannot bind to HER2 receptors. Therefore, our analysis upon ADAM10 expression and miR-122-5p was a good point to understand molecular mechanism of breast cancer. In our study, we investigated the expression profiles of miR-122-5p and its target ADAM10 in 71 breast cancer patients. Immunohistochemical analysis of ER, PR and HER2 gene products was used to categorize tumors in patients. Expression data and immunohistochemical findings were evaluated to comment on the relationship between miR-122-5p and ADAM10. ADAM10 expression was higher in tumor than that of normal tissue but miR-122-5p expression was lower in tumor than that of normal tissue. The expression pattern in HER2+ patients was reverse of the overall result. It can be explained like that miR-122-5p expression increases especially in HER2+ cancer cell to suppress ADAM10 shedding activity on HER2 receptor. However, increase in expression of tumor suppressor miR-122-5p is not enough to inhibit ADAM10. All in all, we can think miR-122-5p as potential regulator of ADAM10 and trastuzumab resistance. Since if we increase miR-122-5p activity together with trastuzumab administration, then HER2+ breast cancer cells may overcome trastuzumab resistance by inhibiting ADAM10 shedding activity on HER2 receptors and increase the efficiency of trastuzumab.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-014-3793-2</identifier><identifier>PMID: 25318895</identifier><language>eng</language><publisher>Dordrecht: Springer-Verlag</publisher><subject>3' Untranslated Regions ; ADAM Proteins - genetics ; ADAM10 Protein ; Adult ; Aged ; Amyloid Precursor Protein Secretases - genetics ; Animal Anatomy ; Animal Biochemistry ; Base Sequence ; Binding Sites ; Biomarkers, Tumor ; Biomedical and Life Sciences ; Breast cancer ; breast neoplasms ; Breast Neoplasms - genetics ; Breast Neoplasms - surgery ; Epidermal growth factor ; Female ; Gene Expression Regulation, Neoplastic ; genes ; Histology ; Humans ; immunohistochemistry ; Life Sciences ; Membrane Proteins - genetics ; microRNA ; MicroRNAs ; MicroRNAs - chemistry ; MicroRNAs - genetics ; Middle Aged ; Molecular biology ; Morphology ; Neoplasm Staging ; patients ; Proteins ; receptors ; RNA Interference ; RNA, Messenger - chemistry ; RNA, Messenger - genetics</subject><ispartof>Molecular biology reports, 2015-02, Vol.42 (2), p.497-505</ispartof><rights>Springer Science+Business Media Dordrecht 2014</rights><rights>Springer Science+Business Media Dordrecht 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-d0b50340bebabaa12bfc61c278b4dde9d9877dcda0d1751cf5c70809179bf1bc3</citedby><cites>FETCH-LOGICAL-c466t-d0b50340bebabaa12bfc61c278b4dde9d9877dcda0d1751cf5c70809179bf1bc3</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/s11033-014-3793-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-014-3793-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25318895$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ergün, Sercan</creatorcontrib><creatorcontrib>Ulasli, Mustafa</creatorcontrib><creatorcontrib>Igci, Yusuf Ziya</creatorcontrib><creatorcontrib>Igci, Mehri</creatorcontrib><creatorcontrib>Kırkbes, Sevil</creatorcontrib><creatorcontrib>Borazan, Ersin</creatorcontrib><creatorcontrib>Balik, Ahmet</creatorcontrib><creatorcontrib>Yumrutaş, Önder</creatorcontrib><creatorcontrib>Camci, Celalettin</creatorcontrib><creatorcontrib>Cakmak, Ecir Ali</creatorcontrib><creatorcontrib>Arslan, Ahmet</creatorcontrib><creatorcontrib>Oztuzcu, Serdar</creatorcontrib><title>association of the expression of miR-122-5p and its target ADAM10 with human breast cancer</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>MicroRNAs can regulate many biological functions. miR-122-5p has a tumor suppressor function through different molecular pathways. Also, our second hit, ADAM10, targeted by miR-122-5p, is a major determinant of HER2 shedding causing that trastuzumab cannot bind to HER2 receptors. Therefore, our analysis upon ADAM10 expression and miR-122-5p was a good point to understand molecular mechanism of breast cancer. In our study, we investigated the expression profiles of miR-122-5p and its target ADAM10 in 71 breast cancer patients. Immunohistochemical analysis of ER, PR and HER2 gene products was used to categorize tumors in patients. Expression data and immunohistochemical findings were evaluated to comment on the relationship between miR-122-5p and ADAM10. ADAM10 expression was higher in tumor than that of normal tissue but miR-122-5p expression was lower in tumor than that of normal tissue. The expression pattern in HER2+ patients was reverse of the overall result. It can be explained like that miR-122-5p expression increases especially in HER2+ cancer cell to suppress ADAM10 shedding activity on HER2 receptor. However, increase in expression of tumor suppressor miR-122-5p is not enough to inhibit ADAM10. All in all, we can think miR-122-5p as potential regulator of ADAM10 and trastuzumab resistance. Since if we increase miR-122-5p activity together with trastuzumab administration, then HER2+ breast cancer cells may overcome trastuzumab resistance by inhibiting ADAM10 shedding activity on HER2 receptors and increase the efficiency of trastuzumab.</description><subject>3' Untranslated Regions</subject><subject>ADAM Proteins - genetics</subject><subject>ADAM10 Protein</subject><subject>Adult</subject><subject>Aged</subject><subject>Amyloid Precursor Protein Secretases - genetics</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Biomarkers, Tumor</subject><subject>Biomedical and Life Sciences</subject><subject>Breast cancer</subject><subject>breast neoplasms</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - surgery</subject><subject>Epidermal growth factor</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>genes</subject><subject>Histology</subject><subject>Humans</subject><subject>immunohistochemistry</subject><subject>Life Sciences</subject><subject>Membrane Proteins - genetics</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - chemistry</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>Molecular biology</subject><subject>Morphology</subject><subject>Neoplasm Staging</subject><subject>patients</subject><subject>Proteins</subject><subject>receptors</subject><subject>RNA Interference</subject><subject>RNA, Messenger - chemistry</subject><subject>RNA, Messenger - genetics</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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>eNp9kU2LFDEQhoMo7rj6A7xowIuXaFXS6aSPw_oJK4K6Fy8hXz3Ty3T3mKRR_70ZehTx4ClQeeqt4ilCHiO8QAD1MiOCEAywYUJ1gvE7ZINSCdZ0St8lGxCArNESL8iDnG8BoEEl75MLLgVq3ckN-Wpznv1gyzBPdO5p2UcafxxTzPlcGYdPDDln8kjtFOhQMi027WKh21fbDwj0-1D2dL-MdqIuRZsL9XbyMT0k93p7yPHR-b0kN29ef7l6x64_vn1_tb1mvmnbwgI4CaIBF5111iJ3vW_Rc6VdE0LsQqeVCj5YCHV59L30CjR0qDrXo_Pikjxfc49p_rbEXMw4ZB8PBzvFeckGW8kbLtuOV_TZP-jtvKSpblepRuu2-mwrhSvl05xzir05pmG06adBMCfxZhVvqnhzEm9OyU_OyYsbY_jT8dt0BfgK5Po17WL6a_R_Up-uTb2djd2lIZubzxxQnk7Z8kr_AkmhlRw</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Ergün, Sercan</creator><creator>Ulasli, Mustafa</creator><creator>Igci, Yusuf Ziya</creator><creator>Igci, Mehri</creator><creator>Kırkbes, Sevil</creator><creator>Borazan, Ersin</creator><creator>Balik, Ahmet</creator><creator>Yumrutaş, Önder</creator><creator>Camci, Celalettin</creator><creator>Cakmak, Ecir Ali</creator><creator>Arslan, Ahmet</creator><creator>Oztuzcu, Serdar</creator><general>Springer-Verlag</general><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>FBQ</scope><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>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150201</creationdate><title>association of the expression of miR-122-5p and its target ADAM10 with human breast cancer</title><author>Ergün, Sercan ; Ulasli, Mustafa ; Igci, Yusuf Ziya ; Igci, Mehri ; Kırkbes, Sevil ; Borazan, Ersin ; Balik, Ahmet ; Yumrutaş, Önder ; Camci, Celalettin ; Cakmak, Ecir Ali ; Arslan, Ahmet ; Oztuzcu, Serdar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-d0b50340bebabaa12bfc61c278b4dde9d9877dcda0d1751cf5c70809179bf1bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>3' Untranslated Regions</topic><topic>ADAM Proteins - 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Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ergün, Sercan</au><au>Ulasli, Mustafa</au><au>Igci, Yusuf Ziya</au><au>Igci, Mehri</au><au>Kırkbes, Sevil</au><au>Borazan, Ersin</au><au>Balik, Ahmet</au><au>Yumrutaş, Önder</au><au>Camci, Celalettin</au><au>Cakmak, Ecir Ali</au><au>Arslan, Ahmet</au><au>Oztuzcu, Serdar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>association of the expression of miR-122-5p and its target ADAM10 with human breast cancer</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>42</volume><issue>2</issue><spage>497</spage><epage>505</epage><pages>497-505</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>MicroRNAs can regulate many biological functions. miR-122-5p has a tumor suppressor function through different molecular pathways. Also, our second hit, ADAM10, targeted by miR-122-5p, is a major determinant of HER2 shedding causing that trastuzumab cannot bind to HER2 receptors. Therefore, our analysis upon ADAM10 expression and miR-122-5p was a good point to understand molecular mechanism of breast cancer. In our study, we investigated the expression profiles of miR-122-5p and its target ADAM10 in 71 breast cancer patients. Immunohistochemical analysis of ER, PR and HER2 gene products was used to categorize tumors in patients. Expression data and immunohistochemical findings were evaluated to comment on the relationship between miR-122-5p and ADAM10. ADAM10 expression was higher in tumor than that of normal tissue but miR-122-5p expression was lower in tumor than that of normal tissue. The expression pattern in HER2+ patients was reverse of the overall result. It can be explained like that miR-122-5p expression increases especially in HER2+ cancer cell to suppress ADAM10 shedding activity on HER2 receptor. However, increase in expression of tumor suppressor miR-122-5p is not enough to inhibit ADAM10. All in all, we can think miR-122-5p as potential regulator of ADAM10 and trastuzumab resistance. Since if we increase miR-122-5p activity together with trastuzumab administration, then HER2+ breast cancer cells may overcome trastuzumab resistance by inhibiting ADAM10 shedding activity on HER2 receptors and increase the efficiency of trastuzumab.</abstract><cop>Dordrecht</cop><pub>Springer-Verlag</pub><pmid>25318895</pmid><doi>10.1007/s11033-014-3793-2</doi><tpages>9</tpages></addata></record> |
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| ispartof | Molecular biology reports, 2015-02, Vol.42 (2), p.497-505 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | 3' Untranslated Regions ADAM Proteins - genetics ADAM10 Protein Adult Aged Amyloid Precursor Protein Secretases - genetics Animal Anatomy Animal Biochemistry Base Sequence Binding Sites Biomarkers, Tumor Biomedical and Life Sciences Breast cancer breast neoplasms Breast Neoplasms - genetics Breast Neoplasms - surgery Epidermal growth factor Female Gene Expression Regulation, Neoplastic genes Histology Humans immunohistochemistry Life Sciences Membrane Proteins - genetics microRNA MicroRNAs MicroRNAs - chemistry MicroRNAs - genetics Middle Aged Molecular biology Morphology Neoplasm Staging patients Proteins receptors RNA Interference RNA, Messenger - chemistry RNA, Messenger - genetics |
| title | association of the expression of miR-122-5p and its target ADAM10 with human breast cancer |
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