FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer
Background Stemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), an...
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| Veröffentlicht in: | Molecular biology reports 2022-04, Vol.49 (4), p.2877-2888 |
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| creator | Modi, Anupama Purohit, Purvi Roy, Dipayan Vishnoi, Jeewan Ram Pareek, Puneet Elhence, Poonam Singh, Priyanka Sharma, Shailja Sharma, Praveen Misra, Sanjeev |
| description | Background
Stemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), and drug resistance (ABCC5) markers were evaluated in BC.
Methods and results
40 diagnosed BC patients and 40 healthy controls were included in this study. Serum GDF-15 was significantly raised (
p
|
| doi_str_mv | 10.1007/s11033-021-07102-5 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2622474503</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2622474503</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-52f6a35d4a38d4c85bfeb61bf809af7c4b986e86d223b0785ec9d6a626c67e243</originalsourceid><addsrcrecordid>eNp9kD1PHDEQhi0UBJeDP0ARWUqTxuBv75aI5AgSiAYEneW1Z9GiO9_h2S3495gcBImCajSaZ94ZPYQcCX4sOHcnKARXinEpGHeCS2Z2yEwYp5huXfONzLjigunGiH3yHfGRc66FM3tkXxlurbN2Ru4W1_dXgq4gDWEEpOe_F0wYmmADOUEeKY6wyoBIQ050yGMZMg6RpjI90AI44BhyhDqhXYGAI42vfTkgu31YIhy-1Tm5Xfy5OfvLLq_PL85OL1lUzozMyN4GZZIOqkk6NqbrobOi6xveht5F3bWNhcYmKVXHXWMgtskGK220DqRWc_Jrm7sp66cJcPSrASMslyHDekIvrZTaaVNFzcnPT-jjeiq5flcp1QqprWkrJbdULGvEAr3flGEVyrMX3L9q91vtvmr3_7R7U5d-vEVPXVX5f-XdcwXUFsA6yg9QPm5_EfsCxqKLow</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2639124659</pqid></control><display><type>article</type><title>FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Modi, Anupama ; Purohit, Purvi ; Roy, Dipayan ; Vishnoi, Jeewan Ram ; Pareek, Puneet ; Elhence, Poonam ; Singh, Priyanka ; Sharma, Shailja ; Sharma, Praveen ; Misra, Sanjeev</creator><creatorcontrib>Modi, Anupama ; Purohit, Purvi ; Roy, Dipayan ; Vishnoi, Jeewan Ram ; Pareek, Puneet ; Elhence, Poonam ; Singh, Priyanka ; Sharma, Shailja ; Sharma, Praveen ; Misra, Sanjeev</creatorcontrib><description>Background
Stemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), and drug resistance (ABCC5) markers were evaluated in BC.
Methods and results
40 diagnosed BC patients and 40 healthy controls were included in this study. Serum GDF-15 was significantly raised (
p
< 0.001) in BC patients. Expressions of GDF-15, OCT4, SOX2, and FOXM1 in BC tissue and cell lines (MCF-7 and MDA-MB-231) were determined by RT-PCR, while phosphorylated AKT (p-AKT) was analyzed by Western blot. Not only were the fold change expressions higher in cancer tissue as compared to surrounding control tissue, but a higher expression was observed for all the genes along with p-AKT in MDA-MB-231 cells compared to MCF-7. Tissue GDF-15 was significantly associated with ABCC5 (
p
< 0.001), OCT4 (
p
= 0.002), SOX2 (
p
< 0.001), and FOXM1 (
p
< 0.001). To further analyze the signaling pathway involved in stemness and drug resistance in BC, GDF-15 knockdown was performed, which reduced the expression of p-AKT, FOXM1, OCT4 and SOX2, and ABCC5, whereas recombinant GDF-15 treatment reversed the same. In silico analyses in UALCAN revealed a similar picture for these genes to that of BC tissue expression.
Conclusions
GDF-15 promotes stemness and intrinsic drug resistance in BC, possibly mediated by the p-AKT/FOXM1 axis.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-021-07102-5</identifier><identifier>PMID: 35066766</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>AKT protein ; Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell Line, Tumor ; Chemoresistance ; Drug resistance ; Drug Resistance, Neoplasm ; Female ; Forkhead Box Protein M1 - genetics ; Growth Differentiation Factor 15 - metabolism ; Growth Differentiation Factor 15 - therapeutic use ; Histology ; Humans ; Life Sciences ; Morphology ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Oct-4 protein ; Original Article ; Patients ; Polymerase chain reaction ; Signal transduction</subject><ispartof>Molecular biology reports, 2022-04, Vol.49 (4), p.2877-2888</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-52f6a35d4a38d4c85bfeb61bf809af7c4b986e86d223b0785ec9d6a626c67e243</citedby><cites>FETCH-LOGICAL-c375t-52f6a35d4a38d4c85bfeb61bf809af7c4b986e86d223b0785ec9d6a626c67e243</cites><orcidid>0000-0002-5928-6280 ; 0000-0001-8559-2911 ; 0000-0002-3429-1470 ; 0000-0002-6488-4701 ; 0000-0002-8324-737X</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/s11033-021-07102-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-021-07102-5$$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/35066766$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Modi, Anupama</creatorcontrib><creatorcontrib>Purohit, Purvi</creatorcontrib><creatorcontrib>Roy, Dipayan</creatorcontrib><creatorcontrib>Vishnoi, Jeewan Ram</creatorcontrib><creatorcontrib>Pareek, Puneet</creatorcontrib><creatorcontrib>Elhence, Poonam</creatorcontrib><creatorcontrib>Singh, Priyanka</creatorcontrib><creatorcontrib>Sharma, Shailja</creatorcontrib><creatorcontrib>Sharma, Praveen</creatorcontrib><creatorcontrib>Misra, Sanjeev</creatorcontrib><title>FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Background
Stemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), and drug resistance (ABCC5) markers were evaluated in BC.
Methods and results
40 diagnosed BC patients and 40 healthy controls were included in this study. Serum GDF-15 was significantly raised (
p
< 0.001) in BC patients. Expressions of GDF-15, OCT4, SOX2, and FOXM1 in BC tissue and cell lines (MCF-7 and MDA-MB-231) were determined by RT-PCR, while phosphorylated AKT (p-AKT) was analyzed by Western blot. Not only were the fold change expressions higher in cancer tissue as compared to surrounding control tissue, but a higher expression was observed for all the genes along with p-AKT in MDA-MB-231 cells compared to MCF-7. Tissue GDF-15 was significantly associated with ABCC5 (
p
< 0.001), OCT4 (
p
= 0.002), SOX2 (
p
< 0.001), and FOXM1 (
p
< 0.001). To further analyze the signaling pathway involved in stemness and drug resistance in BC, GDF-15 knockdown was performed, which reduced the expression of p-AKT, FOXM1, OCT4 and SOX2, and ABCC5, whereas recombinant GDF-15 treatment reversed the same. In silico analyses in UALCAN revealed a similar picture for these genes to that of BC tissue expression.
Conclusions
GDF-15 promotes stemness and intrinsic drug resistance in BC, possibly mediated by the p-AKT/FOXM1 axis.</description><subject>AKT protein</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell Line, Tumor</subject><subject>Chemoresistance</subject><subject>Drug resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Female</subject><subject>Forkhead Box Protein M1 - genetics</subject><subject>Growth Differentiation Factor 15 - metabolism</subject><subject>Growth Differentiation Factor 15 - therapeutic use</subject><subject>Histology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Morphology</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Oct-4 protein</subject><subject>Original Article</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Signal transduction</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</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>eNp9kD1PHDEQhi0UBJeDP0ARWUqTxuBv75aI5AgSiAYEneW1Z9GiO9_h2S3495gcBImCajSaZ94ZPYQcCX4sOHcnKARXinEpGHeCS2Z2yEwYp5huXfONzLjigunGiH3yHfGRc66FM3tkXxlurbN2Ru4W1_dXgq4gDWEEpOe_F0wYmmADOUEeKY6wyoBIQ050yGMZMg6RpjI90AI44BhyhDqhXYGAI42vfTkgu31YIhy-1Tm5Xfy5OfvLLq_PL85OL1lUzozMyN4GZZIOqkk6NqbrobOi6xveht5F3bWNhcYmKVXHXWMgtskGK220DqRWc_Jrm7sp66cJcPSrASMslyHDekIvrZTaaVNFzcnPT-jjeiq5flcp1QqprWkrJbdULGvEAr3flGEVyrMX3L9q91vtvmr3_7R7U5d-vEVPXVX5f-XdcwXUFsA6yg9QPm5_EfsCxqKLow</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Modi, Anupama</creator><creator>Purohit, Purvi</creator><creator>Roy, Dipayan</creator><creator>Vishnoi, Jeewan Ram</creator><creator>Pareek, Puneet</creator><creator>Elhence, Poonam</creator><creator>Singh, Priyanka</creator><creator>Sharma, Shailja</creator><creator>Sharma, Praveen</creator><creator>Misra, Sanjeev</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>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><orcidid>https://orcid.org/0000-0002-5928-6280</orcidid><orcidid>https://orcid.org/0000-0001-8559-2911</orcidid><orcidid>https://orcid.org/0000-0002-3429-1470</orcidid><orcidid>https://orcid.org/0000-0002-6488-4701</orcidid><orcidid>https://orcid.org/0000-0002-8324-737X</orcidid></search><sort><creationdate>20220401</creationdate><title>FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer</title><author>Modi, Anupama ; Purohit, Purvi ; Roy, Dipayan ; Vishnoi, Jeewan Ram ; Pareek, Puneet ; Elhence, Poonam ; Singh, Priyanka ; Sharma, Shailja ; Sharma, Praveen ; Misra, Sanjeev</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-52f6a35d4a38d4c85bfeb61bf809af7c4b986e86d223b0785ec9d6a626c67e243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>AKT protein</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell Line, Tumor</topic><topic>Chemoresistance</topic><topic>Drug resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Female</topic><topic>Forkhead Box Protein M1 - genetics</topic><topic>Growth Differentiation Factor 15 - metabolism</topic><topic>Growth Differentiation Factor 15 - therapeutic use</topic><topic>Histology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Morphology</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Oct-4 protein</topic><topic>Original Article</topic><topic>Patients</topic><topic>Polymerase chain reaction</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Modi, Anupama</creatorcontrib><creatorcontrib>Purohit, Purvi</creatorcontrib><creatorcontrib>Roy, Dipayan</creatorcontrib><creatorcontrib>Vishnoi, Jeewan Ram</creatorcontrib><creatorcontrib>Pareek, Puneet</creatorcontrib><creatorcontrib>Elhence, Poonam</creatorcontrib><creatorcontrib>Singh, Priyanka</creatorcontrib><creatorcontrib>Sharma, Shailja</creatorcontrib><creatorcontrib>Sharma, Praveen</creatorcontrib><creatorcontrib>Misra, Sanjeev</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>Neurosciences Abstracts</collection><collection>Nucleic Acids 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>Science 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>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>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>Science 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>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Modi, Anupama</au><au>Purohit, Purvi</au><au>Roy, Dipayan</au><au>Vishnoi, Jeewan Ram</au><au>Pareek, Puneet</au><au>Elhence, Poonam</au><au>Singh, Priyanka</au><au>Sharma, Shailja</au><au>Sharma, Praveen</au><au>Misra, Sanjeev</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>49</volume><issue>4</issue><spage>2877</spage><epage>2888</epage><pages>2877-2888</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Background
Stemness, a key component of breast cancer (BC) heterogeneity, is responsible for chemoresistance. Growth differentiation factor-15 (GDF-15) induces drug resistance and stemness in BC cells. In this study, the expressions and interactions of GDF-15, FOXM1, and stemness (OCT4 and SOX2), and drug resistance (ABCC5) markers were evaluated in BC.
Methods and results
40 diagnosed BC patients and 40 healthy controls were included in this study. Serum GDF-15 was significantly raised (
p
< 0.001) in BC patients. Expressions of GDF-15, OCT4, SOX2, and FOXM1 in BC tissue and cell lines (MCF-7 and MDA-MB-231) were determined by RT-PCR, while phosphorylated AKT (p-AKT) was analyzed by Western blot. Not only were the fold change expressions higher in cancer tissue as compared to surrounding control tissue, but a higher expression was observed for all the genes along with p-AKT in MDA-MB-231 cells compared to MCF-7. Tissue GDF-15 was significantly associated with ABCC5 (
p
< 0.001), OCT4 (
p
= 0.002), SOX2 (
p
< 0.001), and FOXM1 (
p
< 0.001). To further analyze the signaling pathway involved in stemness and drug resistance in BC, GDF-15 knockdown was performed, which reduced the expression of p-AKT, FOXM1, OCT4 and SOX2, and ABCC5, whereas recombinant GDF-15 treatment reversed the same. In silico analyses in UALCAN revealed a similar picture for these genes to that of BC tissue expression.
Conclusions
GDF-15 promotes stemness and intrinsic drug resistance in BC, possibly mediated by the p-AKT/FOXM1 axis.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>35066766</pmid><doi>10.1007/s11033-021-07102-5</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-5928-6280</orcidid><orcidid>https://orcid.org/0000-0001-8559-2911</orcidid><orcidid>https://orcid.org/0000-0002-3429-1470</orcidid><orcidid>https://orcid.org/0000-0002-6488-4701</orcidid><orcidid>https://orcid.org/0000-0002-8324-737X</orcidid></addata></record> |
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| ispartof | Molecular biology reports, 2022-04, Vol.49 (4), p.2877-2888 |
| issn | 0301-4851 1573-4978 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | AKT protein Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell Line, Tumor Chemoresistance Drug resistance Drug Resistance, Neoplasm Female Forkhead Box Protein M1 - genetics Growth Differentiation Factor 15 - metabolism Growth Differentiation Factor 15 - therapeutic use Histology Humans Life Sciences Morphology Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Oct-4 protein Original Article Patients Polymerase chain reaction Signal transduction |
| title | FOXM1 mediates GDF-15 dependent stemness and intrinsic drug resistance in breast cancer |
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