Bile acid: a potential inducer of colon cancer stem cells
Although the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids m...
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| Veröffentlicht in: | Stem cell research & therapy 2016-12, Vol.7 (1), p.181-181, Article 181 |
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| creator | Farhana, Lulu Nangia-Makker, Pratima Arbit, Evan Shango, Kathren Sarkar, Sarah Mahmud, Hamidah Hadden, Timothy Yu, Yingjie Majumdar, Adhip P N |
| description | Although the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids may promote stemness in colonic epithelial cells leading to generation of cancer stem cells (CSCs) that play a role in the development and progression of colon cancer.
Normal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs. The expression of CSC markers was measured by real-time qPCR. Flow cytometry was used to isolate CSCs. T-cell factor/lymphoid-enhancing factor (TCF/LEF) luciferase assay was employed to examine the transcriptional activity of β-catenin. Downregulation of muscarinic 3 receptor (M3R) was achieved through transfection of corresponding siRNA.
We found DCA/LCA to induce CSCs in normal human colonic epithelial cells, as evidenced by the increased proportion of CSCs, elevated levels of several CSC markers, as well as a number of epithelial-mesenchymal transition markers together with increased colonosphere formation, drug exclusion, ABCB1 and ABCG2 expression, and induction of M3R, p-EGFR, matrix metallopeptidases, and c-Myc. Inhibition of M3R signaling greatly suppressed DCA/LCA induction of the CSC marker ALDHA1 and also c-Myc mRNA expression as well as transcriptional activation of TCF/LEF.
Our results suggest that bile acids, specifically DCA and LCA, induce cancer stemness in colonic epithelial cells by modulating M3R and Wnt/β-catenin signaling and thus could be considered promoters of colon cancer. |
| doi_str_mv | 10.1186/s13287-016-0439-4 |
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Normal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs. The expression of CSC markers was measured by real-time qPCR. Flow cytometry was used to isolate CSCs. T-cell factor/lymphoid-enhancing factor (TCF/LEF) luciferase assay was employed to examine the transcriptional activity of β-catenin. Downregulation of muscarinic 3 receptor (M3R) was achieved through transfection of corresponding siRNA.
We found DCA/LCA to induce CSCs in normal human colonic epithelial cells, as evidenced by the increased proportion of CSCs, elevated levels of several CSC markers, as well as a number of epithelial-mesenchymal transition markers together with increased colonosphere formation, drug exclusion, ABCB1 and ABCG2 expression, and induction of M3R, p-EGFR, matrix metallopeptidases, and c-Myc. Inhibition of M3R signaling greatly suppressed DCA/LCA induction of the CSC marker ALDHA1 and also c-Myc mRNA expression as well as transcriptional activation of TCF/LEF.
Our results suggest that bile acids, specifically DCA and LCA, induce cancer stemness in colonic epithelial cells by modulating M3R and Wnt/β-catenin signaling and thus could be considered promoters of colon cancer.</description><identifier>ISSN: 1757-6512</identifier><identifier>EISSN: 1757-6512</identifier><identifier>DOI: 10.1186/s13287-016-0439-4</identifier><identifier>PMID: 27908290</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; ATP Binding Cassette Transporter, Sub-Family B - genetics ; ATP Binding Cassette Transporter, Sub-Family B - metabolism ; ATP Binding Cassette Transporter, Sub-Family G, Member 2 - genetics ; ATP Binding Cassette Transporter, Sub-Family G, Member 2 - metabolism ; beta Catenin - genetics ; beta Catenin - metabolism ; Bile acids ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Cell Line ; Cell Transformation, Neoplastic - drug effects ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Colon - drug effects ; Colon - metabolism ; Colon - pathology ; Colon cancer ; Complications and side effects ; Deoxycholic Acid - pharmacology ; Development and progression ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Humans ; Lithocholic Acid - pharmacology ; Luciferases - genetics ; Luciferases - metabolism ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Proto-Oncogene Proteins c-myc - genetics ; Proto-Oncogene Proteins c-myc - metabolism ; Receptor, Epidermal Growth Factor - genetics ; Receptor, Epidermal Growth Factor - metabolism ; Receptor, Muscarinic M3 - antagonists & inhibitors ; Receptor, Muscarinic M3 - genetics ; Receptor, Muscarinic M3 - metabolism ; Risk factors ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; Signal Transduction ; Stem cells ; T Cell Transcription Factor 1 - genetics ; T Cell Transcription Factor 1 - metabolism</subject><ispartof>Stem cell research & therapy, 2016-12, Vol.7 (1), p.181-181, Article 181</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c625t-b54098ca341ec1e89502d8cfc5c9c3469460ca6d7f295ac0d84fc5b14a21a0523</citedby><cites>FETCH-LOGICAL-c625t-b54098ca341ec1e89502d8cfc5c9c3469460ca6d7f295ac0d84fc5b14a21a0523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5134122/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5134122/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27908290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Farhana, Lulu</creatorcontrib><creatorcontrib>Nangia-Makker, Pratima</creatorcontrib><creatorcontrib>Arbit, Evan</creatorcontrib><creatorcontrib>Shango, Kathren</creatorcontrib><creatorcontrib>Sarkar, Sarah</creatorcontrib><creatorcontrib>Mahmud, Hamidah</creatorcontrib><creatorcontrib>Hadden, Timothy</creatorcontrib><creatorcontrib>Yu, Yingjie</creatorcontrib><creatorcontrib>Majumdar, Adhip P N</creatorcontrib><title>Bile acid: a potential inducer of colon cancer stem cells</title><title>Stem cell research & therapy</title><addtitle>Stem Cell Res Ther</addtitle><description>Although the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids may promote stemness in colonic epithelial cells leading to generation of cancer stem cells (CSCs) that play a role in the development and progression of colon cancer.
Normal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs. The expression of CSC markers was measured by real-time qPCR. Flow cytometry was used to isolate CSCs. T-cell factor/lymphoid-enhancing factor (TCF/LEF) luciferase assay was employed to examine the transcriptional activity of β-catenin. Downregulation of muscarinic 3 receptor (M3R) was achieved through transfection of corresponding siRNA.
We found DCA/LCA to induce CSCs in normal human colonic epithelial cells, as evidenced by the increased proportion of CSCs, elevated levels of several CSC markers, as well as a number of epithelial-mesenchymal transition markers together with increased colonosphere formation, drug exclusion, ABCB1 and ABCG2 expression, and induction of M3R, p-EGFR, matrix metallopeptidases, and c-Myc. Inhibition of M3R signaling greatly suppressed DCA/LCA induction of the CSC marker ALDHA1 and also c-Myc mRNA expression as well as transcriptional activation of TCF/LEF.
Our results suggest that bile acids, specifically DCA and LCA, induce cancer stemness in colonic epithelial cells by modulating M3R and Wnt/β-catenin signaling and thus could be considered promoters of colon cancer.</description><subject>Analysis</subject><subject>ATP Binding Cassette Transporter, Sub-Family B - genetics</subject><subject>ATP Binding Cassette Transporter, Sub-Family B - metabolism</subject><subject>ATP Binding Cassette Transporter, Sub-Family G, Member 2 - genetics</subject><subject>ATP Binding Cassette Transporter, Sub-Family G, Member 2 - metabolism</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Bile acids</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Cell Line</subject><subject>Cell Transformation, Neoplastic - drug effects</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Colon - drug effects</subject><subject>Colon - metabolism</subject><subject>Colon - pathology</subject><subject>Colon cancer</subject><subject>Complications and side effects</subject><subject>Deoxycholic Acid - pharmacology</subject><subject>Development and progression</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Reporter</subject><subject>Humans</subject><subject>Lithocholic Acid - pharmacology</subject><subject>Luciferases - genetics</subject><subject>Luciferases - metabolism</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptor, Muscarinic M3 - antagonists & inhibitors</subject><subject>Receptor, Muscarinic M3 - genetics</subject><subject>Receptor, Muscarinic M3 - metabolism</subject><subject>Risk factors</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>T Cell Transcription Factor 1 - genetics</subject><subject>T Cell Transcription Factor 1 - metabolism</subject><issn>1757-6512</issn><issn>1757-6512</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</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>eNptkl1rFDEUhoMottT-AG9kQBC9mJrvSbwo1KK2UBD8uA7ZTGY3JZOsk4zYf9-Ere1OaXKRhPOc9-QcXgBeI3iCkOAfEyJYdC1EvIWUyJY-A4eoY13LGcLP9-4H4Dila1gWIRBy-hIc4E5CgSU8BPKz87bRxvWfGt1sY7YhO-0bF_rZ2KmJQ2Oij6ExOtR3ynZsjPU-vQIvBu2TPb47j8Dvr19-nV-0V9-_XZ6fXbWGY5bbFaNQCqMJRdYgKySDuBdmMMxIQyiXlEOjed8NWDJtYC9oia0Q1RhpyDA5Aqc73e28Gm1vygcn7dV2cqOeblTUTi0jwW3UOv5VDJWauAq8vxOY4p_ZpqxGl2oLOtg4J4UEZQJjiWlB3z5Cr-M8hdJepTiVlHD4QK21t8qFIZa6poqqM9phhruuq1onT1Bl93Z0JgY7lMkvEz4sEgqT7b-81nNK6vLnjyX7bo_dWO3zJkU_ZxdDWoJoB5oppjTZ4X5wCKrqI7XzkSo-UtVHqua82Z_4fcZ_15BbzH--SQ</recordid><startdate>20161201</startdate><enddate>20161201</enddate><creator>Farhana, Lulu</creator><creator>Nangia-Makker, Pratima</creator><creator>Arbit, Evan</creator><creator>Shango, Kathren</creator><creator>Sarkar, Sarah</creator><creator>Mahmud, Hamidah</creator><creator>Hadden, Timothy</creator><creator>Yu, Yingjie</creator><creator>Majumdar, Adhip P N</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ISR</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161201</creationdate><title>Bile acid: a potential inducer of colon cancer stem cells</title><author>Farhana, Lulu ; Nangia-Makker, Pratima ; Arbit, Evan ; Shango, Kathren ; Sarkar, Sarah ; Mahmud, Hamidah ; Hadden, Timothy ; Yu, Yingjie ; Majumdar, Adhip P N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c625t-b54098ca341ec1e89502d8cfc5c9c3469460ca6d7f295ac0d84fc5b14a21a0523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Analysis</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - genetics</topic><topic>ATP Binding Cassette Transporter, Sub-Family B - metabolism</topic><topic>ATP Binding Cassette Transporter, Sub-Family G, Member 2 - genetics</topic><topic>ATP Binding Cassette Transporter, Sub-Family G, Member 2 - metabolism</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Bile acids</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Cell Line</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Colon - drug effects</topic><topic>Colon - metabolism</topic><topic>Colon - pathology</topic><topic>Colon cancer</topic><topic>Complications and side effects</topic><topic>Deoxycholic Acid - pharmacology</topic><topic>Development and progression</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Epithelial Cells - pathology</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Reporter</topic><topic>Humans</topic><topic>Lithocholic Acid - pharmacology</topic><topic>Luciferases - genetics</topic><topic>Luciferases - metabolism</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Proto-Oncogene Proteins c-myc - genetics</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Receptor, Muscarinic M3 - antagonists & inhibitors</topic><topic>Receptor, Muscarinic M3 - genetics</topic><topic>Receptor, Muscarinic M3 - metabolism</topic><topic>Risk factors</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction</topic><topic>Stem cells</topic><topic>T Cell Transcription Factor 1 - genetics</topic><topic>T Cell Transcription Factor 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Farhana, Lulu</creatorcontrib><creatorcontrib>Nangia-Makker, Pratima</creatorcontrib><creatorcontrib>Arbit, Evan</creatorcontrib><creatorcontrib>Shango, Kathren</creatorcontrib><creatorcontrib>Sarkar, Sarah</creatorcontrib><creatorcontrib>Mahmud, Hamidah</creatorcontrib><creatorcontrib>Hadden, Timothy</creatorcontrib><creatorcontrib>Yu, Yingjie</creatorcontrib><creatorcontrib>Majumdar, Adhip P N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>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>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Stem cell research & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Farhana, Lulu</au><au>Nangia-Makker, Pratima</au><au>Arbit, Evan</au><au>Shango, Kathren</au><au>Sarkar, Sarah</au><au>Mahmud, Hamidah</au><au>Hadden, Timothy</au><au>Yu, Yingjie</au><au>Majumdar, Adhip P N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bile acid: a potential inducer of colon cancer stem cells</atitle><jtitle>Stem cell research & therapy</jtitle><addtitle>Stem Cell Res Ther</addtitle><date>2016-12-01</date><risdate>2016</risdate><volume>7</volume><issue>1</issue><spage>181</spage><epage>181</epage><pages>181-181</pages><artnum>181</artnum><issn>1757-6512</issn><eissn>1757-6512</eissn><abstract>Although the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids may promote stemness in colonic epithelial cells leading to generation of cancer stem cells (CSCs) that play a role in the development and progression of colon cancer.
Normal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs. The expression of CSC markers was measured by real-time qPCR. Flow cytometry was used to isolate CSCs. T-cell factor/lymphoid-enhancing factor (TCF/LEF) luciferase assay was employed to examine the transcriptional activity of β-catenin. Downregulation of muscarinic 3 receptor (M3R) was achieved through transfection of corresponding siRNA.
We found DCA/LCA to induce CSCs in normal human colonic epithelial cells, as evidenced by the increased proportion of CSCs, elevated levels of several CSC markers, as well as a number of epithelial-mesenchymal transition markers together with increased colonosphere formation, drug exclusion, ABCB1 and ABCG2 expression, and induction of M3R, p-EGFR, matrix metallopeptidases, and c-Myc. Inhibition of M3R signaling greatly suppressed DCA/LCA induction of the CSC marker ALDHA1 and also c-Myc mRNA expression as well as transcriptional activation of TCF/LEF.
Our results suggest that bile acids, specifically DCA and LCA, induce cancer stemness in colonic epithelial cells by modulating M3R and Wnt/β-catenin signaling and thus could be considered promoters of colon cancer.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27908290</pmid><doi>10.1186/s13287-016-0439-4</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; SpringerNature Journals; PubMed Central Open Access; Springer Nature OA Free Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Analysis ATP Binding Cassette Transporter, Sub-Family B - genetics ATP Binding Cassette Transporter, Sub-Family B - metabolism ATP Binding Cassette Transporter, Sub-Family G, Member 2 - genetics ATP Binding Cassette Transporter, Sub-Family G, Member 2 - metabolism beta Catenin - genetics beta Catenin - metabolism Bile acids Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Cell Line Cell Transformation, Neoplastic - drug effects Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Colon - drug effects Colon - metabolism Colon - pathology Colon cancer Complications and side effects Deoxycholic Acid - pharmacology Development and progression Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation, Neoplastic Genes, Reporter Humans Lithocholic Acid - pharmacology Luciferases - genetics Luciferases - metabolism Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Receptor, Muscarinic M3 - antagonists & inhibitors Receptor, Muscarinic M3 - genetics Receptor, Muscarinic M3 - metabolism Risk factors RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Signal Transduction Stem cells T Cell Transcription Factor 1 - genetics T Cell Transcription Factor 1 - metabolism |
| title | Bile acid: a potential inducer of colon cancer stem cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T10%3A27%3A43IST&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=Bile%20acid:%20a%20potential%20inducer%20of%20colon%20cancer%20stem%20cells&rft.jtitle=Stem%20cell%20research%20&%20therapy&rft.au=Farhana,%20Lulu&rft.date=2016-12-01&rft.volume=7&rft.issue=1&rft.spage=181&rft.epage=181&rft.pages=181-181&rft.artnum=181&rft.issn=1757-6512&rft.eissn=1757-6512&rft_id=info:doi/10.1186/s13287-016-0439-4&rft_dat=%3Cgale_pubme%3EA472527774%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=1846494360&rft_id=info:pmid/27908290&rft_galeid=A472527774&rfr_iscdi=true |