ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness
Purpose Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer which could progress to or recur as invasive breast cancer. The underlying molecular mechanism of DCIS progression is yet poorly understood, and appropriate biomarkers to distinguish benign form of DCIS from potentially...
Gespeichert in:
| Veröffentlicht in: | Breast cancer research and treatment 2019-05, Vol.175 (1), p.77-90 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 90 |
|---|---|
| container_issue | 1 |
| container_start_page | 77 |
| container_title | Breast cancer research and treatment |
| container_volume | 175 |
| creator | Liu, Yin Pandey, Puspa R. Sharma, Sambad Xing, Fei Wu, Kerui Chittiboyina, Amar Wu, Shih-Ying Tyagi, Abhishek Watabe, Kounosuke |
| description | Purpose
Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer which could progress to or recur as invasive breast cancer. The underlying molecular mechanism of DCIS progression is yet poorly understood, and appropriate biomarkers to distinguish benign form of DCIS from potentially invasive tumor are urgently needed.
Methods
To identify the key regulators of DCIS progression, we performed gene-expression analysis of syngeneic breast cancer cell lines MCF10A, DCIS.com, and MCF10CA and cross-referenced the targets with patient cohort data.
Results
We identified ID2 as a critical gene for DCIS initiation and found that ID2 promoted DCIS formation by enhancing cancer stemness of pre-malignant cells. ID2 also plays a pivotal role in survival of the aggressive cancer cells. In addition, we identified INHBA and GJB2 as key regulators for the transition of benign DCIS to aggressive phenotype. These two genes regulate migration, colonization, and stemness of invasive cancer cells. Upregulation of ID2 and GJB2 predicts poor prognosis after breast-conserving surgery. Finally, we found a natural compound Helichrysetin as ID2 inhibitor which suppresses DCIS formation in vitro and in vivo.
Conclusion
Our results indicate that ID2 is a key driver of DCIS formation and therefore is considered to be a potential target for prevention of DCIS, while INHBA and GJB2 play vital roles in progression of DCIS to IDC and they may serve as potential prognosis markers. |
| doi_str_mv | 10.1007/s10549-018-05126-3 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6494690</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A584130899</galeid><sourcerecordid>A584130899</sourcerecordid><originalsourceid>FETCH-LOGICAL-c572t-9f2dc6b15ac0abeadfde356e45fef5c2390532a93d47b68155518ff0c4f9d9d93</originalsourceid><addsrcrecordid>eNp9kkuLFDEUhYMoTjv6B1xIgSBuasyjklQ2wsyo48iAGwV3IZW6qa6hKmmTlND_3rQ9rxaRLAK53z2Xe3IQeknwCcFYvksE80bVmLQ15oSKmj1CK8IlqyUl8jFaYSJkLVosjtCzlK4xxkpi9RQdMSwpp4ys0I_LD7Qyvq8uvpzRahPDHDJUYOK0rVM2A1RdBJNyZY23EHfEECGlMfiq21YRhmUyefTDLZAyzL4Az9ETZ6YEL27uY_T908dv55_rq68Xl-enV7XlkuZaOdpb0RFuLDYdmN71wLiAhjtw3FKmMGfUKNY3shMt4ZyT1jlsG6f6ctgxer_X3SzdDL0Fn6OZ9CaOs4lbHcyoDyt-XOsh_NKiUY1QuAi8vRGI4ecCKet5TBamyXgIS9KUFq9b2vDdrNd_oddhib6sp4vhgsuGsPaeGswEevQulLl2J6pPeVsQ3Kqd1sk_qHJ6mEcbPLixvB80vHnQsAYz5XUK05LLV6RDkO5BG0NKEdydGQTrXXD0Pji6BEf_CY5mpenVQxvvWm6TUgC2B1Ip-QHi_e7_kf0N1LzMwg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2176574138</pqid></control><display><type>article</type><title>ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Liu, Yin ; Pandey, Puspa R. ; Sharma, Sambad ; Xing, Fei ; Wu, Kerui ; Chittiboyina, Amar ; Wu, Shih-Ying ; Tyagi, Abhishek ; Watabe, Kounosuke</creator><creatorcontrib>Liu, Yin ; Pandey, Puspa R. ; Sharma, Sambad ; Xing, Fei ; Wu, Kerui ; Chittiboyina, Amar ; Wu, Shih-Ying ; Tyagi, Abhishek ; Watabe, Kounosuke</creatorcontrib><description>Purpose
Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer which could progress to or recur as invasive breast cancer. The underlying molecular mechanism of DCIS progression is yet poorly understood, and appropriate biomarkers to distinguish benign form of DCIS from potentially invasive tumor are urgently needed.
Methods
To identify the key regulators of DCIS progression, we performed gene-expression analysis of syngeneic breast cancer cell lines MCF10A, DCIS.com, and MCF10CA and cross-referenced the targets with patient cohort data.
Results
We identified ID2 as a critical gene for DCIS initiation and found that ID2 promoted DCIS formation by enhancing cancer stemness of pre-malignant cells. ID2 also plays a pivotal role in survival of the aggressive cancer cells. In addition, we identified INHBA and GJB2 as key regulators for the transition of benign DCIS to aggressive phenotype. These two genes regulate migration, colonization, and stemness of invasive cancer cells. Upregulation of ID2 and GJB2 predicts poor prognosis after breast-conserving surgery. Finally, we found a natural compound Helichrysetin as ID2 inhibitor which suppresses DCIS formation in vitro and in vivo.
Conclusion
Our results indicate that ID2 is a key driver of DCIS formation and therefore is considered to be a potential target for prevention of DCIS, while INHBA and GJB2 play vital roles in progression of DCIS to IDC and they may serve as potential prognosis markers.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-018-05126-3</identifier><identifier>PMID: 30725231</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analysis ; Animals ; Benign ; Biological markers ; Biomarkers, Tumor ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - mortality ; Breast Neoplasms - pathology ; Cancer cells ; Cancer research ; Carcinoma ; Carcinoma, Intraductal, Noninfiltrating - genetics ; Carcinoma, Intraductal, Noninfiltrating - pathology ; Cell Proliferation ; Chalcone - analogs & derivatives ; Chalcone - chemistry ; Chalcone - pharmacology ; Colonization ; Connexins - genetics ; Disease Models, Animal ; Disease Progression ; Female ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes ; Heterografts ; Humans ; Inhibins ; Inhibitor of Differentiation Protein 2 - genetics ; Lumpectomy ; Mastectomy ; Medical prognosis ; Medical schools ; Medicine ; Medicine & Public Health ; Mice ; Neoplasm Staging ; Neoplastic Stem Cells - metabolism ; Oncology ; Phenotypes ; Preclinical Study ; Prognosis ; Promoter Regions, Genetic ; Recurrence (Disease) ; Surgery ; Tumor cell lines ; Tumors</subject><ispartof>Breast cancer research and treatment, 2019-05, Vol.175 (1), p.77-90</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>COPYRIGHT 2019 Springer</rights><rights>Breast Cancer Research and Treatment is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c572t-9f2dc6b15ac0abeadfde356e45fef5c2390532a93d47b68155518ff0c4f9d9d93</citedby><cites>FETCH-LOGICAL-c572t-9f2dc6b15ac0abeadfde356e45fef5c2390532a93d47b68155518ff0c4f9d9d93</cites><orcidid>0000-0001-7441-6322</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/s10549-018-05126-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-018-05126-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30725231$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yin</creatorcontrib><creatorcontrib>Pandey, Puspa R.</creatorcontrib><creatorcontrib>Sharma, Sambad</creatorcontrib><creatorcontrib>Xing, Fei</creatorcontrib><creatorcontrib>Wu, Kerui</creatorcontrib><creatorcontrib>Chittiboyina, Amar</creatorcontrib><creatorcontrib>Wu, Shih-Ying</creatorcontrib><creatorcontrib>Tyagi, Abhishek</creatorcontrib><creatorcontrib>Watabe, Kounosuke</creatorcontrib><title>ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Purpose
Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer which could progress to or recur as invasive breast cancer. The underlying molecular mechanism of DCIS progression is yet poorly understood, and appropriate biomarkers to distinguish benign form of DCIS from potentially invasive tumor are urgently needed.
Methods
To identify the key regulators of DCIS progression, we performed gene-expression analysis of syngeneic breast cancer cell lines MCF10A, DCIS.com, and MCF10CA and cross-referenced the targets with patient cohort data.
Results
We identified ID2 as a critical gene for DCIS initiation and found that ID2 promoted DCIS formation by enhancing cancer stemness of pre-malignant cells. ID2 also plays a pivotal role in survival of the aggressive cancer cells. In addition, we identified INHBA and GJB2 as key regulators for the transition of benign DCIS to aggressive phenotype. These two genes regulate migration, colonization, and stemness of invasive cancer cells. Upregulation of ID2 and GJB2 predicts poor prognosis after breast-conserving surgery. Finally, we found a natural compound Helichrysetin as ID2 inhibitor which suppresses DCIS formation in vitro and in vivo.
Conclusion
Our results indicate that ID2 is a key driver of DCIS formation and therefore is considered to be a potential target for prevention of DCIS, while INHBA and GJB2 play vital roles in progression of DCIS to IDC and they may serve as potential prognosis markers.</description><subject>Analysis</subject><subject>Animals</subject><subject>Benign</subject><subject>Biological markers</subject><subject>Biomarkers, Tumor</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - mortality</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer cells</subject><subject>Cancer research</subject><subject>Carcinoma</subject><subject>Carcinoma, Intraductal, Noninfiltrating - genetics</subject><subject>Carcinoma, Intraductal, Noninfiltrating - pathology</subject><subject>Cell Proliferation</subject><subject>Chalcone - analogs & derivatives</subject><subject>Chalcone - chemistry</subject><subject>Chalcone - pharmacology</subject><subject>Colonization</subject><subject>Connexins - genetics</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Inhibins</subject><subject>Inhibitor of Differentiation Protein 2 - genetics</subject><subject>Lumpectomy</subject><subject>Mastectomy</subject><subject>Medical prognosis</subject><subject>Medical schools</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Neoplasm Staging</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Oncology</subject><subject>Phenotypes</subject><subject>Preclinical Study</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic</subject><subject>Recurrence (Disease)</subject><subject>Surgery</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kkuLFDEUhYMoTjv6B1xIgSBuasyjklQ2wsyo48iAGwV3IZW6qa6hKmmTlND_3rQ9rxaRLAK53z2Xe3IQeknwCcFYvksE80bVmLQ15oSKmj1CK8IlqyUl8jFaYSJkLVosjtCzlK4xxkpi9RQdMSwpp4ys0I_LD7Qyvq8uvpzRahPDHDJUYOK0rVM2A1RdBJNyZY23EHfEECGlMfiq21YRhmUyefTDLZAyzL4Az9ETZ6YEL27uY_T908dv55_rq68Xl-enV7XlkuZaOdpb0RFuLDYdmN71wLiAhjtw3FKmMGfUKNY3shMt4ZyT1jlsG6f6ctgxer_X3SzdDL0Fn6OZ9CaOs4lbHcyoDyt-XOsh_NKiUY1QuAi8vRGI4ecCKet5TBamyXgIS9KUFq9b2vDdrNd_oddhib6sp4vhgsuGsPaeGswEevQulLl2J6pPeVsQ3Kqd1sk_qHJ6mEcbPLixvB80vHnQsAYz5XUK05LLV6RDkO5BG0NKEdydGQTrXXD0Pji6BEf_CY5mpenVQxvvWm6TUgC2B1Ip-QHi_e7_kf0N1LzMwg</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Liu, Yin</creator><creator>Pandey, Puspa R.</creator><creator>Sharma, Sambad</creator><creator>Xing, Fei</creator><creator>Wu, Kerui</creator><creator>Chittiboyina, Amar</creator><creator>Wu, Shih-Ying</creator><creator>Tyagi, Abhishek</creator><creator>Watabe, Kounosuke</creator><general>Springer US</general><general>Springer</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>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7441-6322</orcidid></search><sort><creationdate>20190501</creationdate><title>ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness</title><author>Liu, Yin ; Pandey, Puspa R. ; Sharma, Sambad ; Xing, Fei ; Wu, Kerui ; Chittiboyina, Amar ; Wu, Shih-Ying ; Tyagi, Abhishek ; Watabe, Kounosuke</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c572t-9f2dc6b15ac0abeadfde356e45fef5c2390532a93d47b68155518ff0c4f9d9d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Benign</topic><topic>Biological markers</topic><topic>Biomarkers, Tumor</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - mortality</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer cells</topic><topic>Cancer research</topic><topic>Carcinoma</topic><topic>Carcinoma, Intraductal, Noninfiltrating - genetics</topic><topic>Carcinoma, Intraductal, Noninfiltrating - pathology</topic><topic>Cell Proliferation</topic><topic>Chalcone - analogs & derivatives</topic><topic>Chalcone - chemistry</topic><topic>Chalcone - pharmacology</topic><topic>Colonization</topic><topic>Connexins - genetics</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Inhibins</topic><topic>Inhibitor of Differentiation Protein 2 - genetics</topic><topic>Lumpectomy</topic><topic>Mastectomy</topic><topic>Medical prognosis</topic><topic>Medical schools</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Neoplasm Staging</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Oncology</topic><topic>Phenotypes</topic><topic>Preclinical Study</topic><topic>Prognosis</topic><topic>Promoter Regions, Genetic</topic><topic>Recurrence (Disease)</topic><topic>Surgery</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yin</creatorcontrib><creatorcontrib>Pandey, Puspa R.</creatorcontrib><creatorcontrib>Sharma, Sambad</creatorcontrib><creatorcontrib>Xing, Fei</creatorcontrib><creatorcontrib>Wu, Kerui</creatorcontrib><creatorcontrib>Chittiboyina, Amar</creatorcontrib><creatorcontrib>Wu, Shih-Ying</creatorcontrib><creatorcontrib>Tyagi, Abhishek</creatorcontrib><creatorcontrib>Watabe, Kounosuke</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>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yin</au><au>Pandey, Puspa R.</au><au>Sharma, Sambad</au><au>Xing, Fei</au><au>Wu, Kerui</au><au>Chittiboyina, Amar</au><au>Wu, Shih-Ying</au><au>Tyagi, Abhishek</au><au>Watabe, Kounosuke</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>175</volume><issue>1</issue><spage>77</spage><epage>90</epage><pages>77-90</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><abstract>Purpose
Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer which could progress to or recur as invasive breast cancer. The underlying molecular mechanism of DCIS progression is yet poorly understood, and appropriate biomarkers to distinguish benign form of DCIS from potentially invasive tumor are urgently needed.
Methods
To identify the key regulators of DCIS progression, we performed gene-expression analysis of syngeneic breast cancer cell lines MCF10A, DCIS.com, and MCF10CA and cross-referenced the targets with patient cohort data.
Results
We identified ID2 as a critical gene for DCIS initiation and found that ID2 promoted DCIS formation by enhancing cancer stemness of pre-malignant cells. ID2 also plays a pivotal role in survival of the aggressive cancer cells. In addition, we identified INHBA and GJB2 as key regulators for the transition of benign DCIS to aggressive phenotype. These two genes regulate migration, colonization, and stemness of invasive cancer cells. Upregulation of ID2 and GJB2 predicts poor prognosis after breast-conserving surgery. Finally, we found a natural compound Helichrysetin as ID2 inhibitor which suppresses DCIS formation in vitro and in vivo.
Conclusion
Our results indicate that ID2 is a key driver of DCIS formation and therefore is considered to be a potential target for prevention of DCIS, while INHBA and GJB2 play vital roles in progression of DCIS to IDC and they may serve as potential prognosis markers.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30725231</pmid><doi>10.1007/s10549-018-05126-3</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7441-6322</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0167-6806 |
| ispartof | Breast cancer research and treatment, 2019-05, Vol.175 (1), p.77-90 |
| issn | 0167-6806 1573-7217 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6494690 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Analysis Animals Benign Biological markers Biomarkers, Tumor Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - mortality Breast Neoplasms - pathology Cancer cells Cancer research Carcinoma Carcinoma, Intraductal, Noninfiltrating - genetics Carcinoma, Intraductal, Noninfiltrating - pathology Cell Proliferation Chalcone - analogs & derivatives Chalcone - chemistry Chalcone - pharmacology Colonization Connexins - genetics Disease Models, Animal Disease Progression Female Gene expression Gene Expression Profiling Gene Expression Regulation, Neoplastic Genes Heterografts Humans Inhibins Inhibitor of Differentiation Protein 2 - genetics Lumpectomy Mastectomy Medical prognosis Medical schools Medicine Medicine & Public Health Mice Neoplasm Staging Neoplastic Stem Cells - metabolism Oncology Phenotypes Preclinical Study Prognosis Promoter Regions, Genetic Recurrence (Disease) Surgery Tumor cell lines Tumors |
| title | ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T11%3A55%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ID2%20and%20GJB2%20promote%20early-stage%20breast%20cancer%20progression%20by%20regulating%20cancer%20stemness&rft.jtitle=Breast%20cancer%20research%20and%20treatment&rft.au=Liu,%20Yin&rft.date=2019-05-01&rft.volume=175&rft.issue=1&rft.spage=77&rft.epage=90&rft.pages=77-90&rft.issn=0167-6806&rft.eissn=1573-7217&rft_id=info:doi/10.1007/s10549-018-05126-3&rft_dat=%3Cgale_pubme%3EA584130899%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2176574138&rft_id=info:pmid/30725231&rft_galeid=A584130899&rfr_iscdi=true |