p53 regulates epithelial–mesenchymal transition and stem cell properties through modulating miRNAs
The epithelial to mesenchymal transition (EMT) has been recently associated with a stem cell phenotype. In breast cancer cell lines and tumours, p53 directly targets the expression of microRNAs that have been shown to inhibit EMT and stem cells regulators. The epithelial–mesenchymal transition (EMT)...
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| Published in | Nature cell biology Vol. 13; no. 3; pp. 317 - 323 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.03.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The epithelial to mesenchymal transition (EMT) has been recently associated with a stem cell phenotype. In breast cancer cell lines and tumours, p53 directly targets the expression of microRNAs that have been shown to inhibit EMT and stem cells regulators.
The epithelial–mesenchymal transition (EMT) has recently been linked to stem cell phenotype
1
,
2
. However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates
miR-200c
through direct binding to the
miR-200c
promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties
3
,
4
and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT–MET (mesenchymal–epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53–miR-200c pathway. |
|---|---|
| AbstractList | The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype. However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT-MET (mesenchymal-epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53-miR-200c pathway.The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype. However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT-MET (mesenchymal-epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53-miR-200c pathway. The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype. However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT-MET (mesenchymal-epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53-miR-200c pathway. Epithelial mechenchymal transition (EMT) has recently been linked to stem cell phenotype 1 , 2 . However, the molecular mechanism involving regulation of EMT and stemness remains elusive. Here, using genomic approaches, we discovered that tumor suppressor p53 plays a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates EMT program, accompanied by increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties 3 , 4 and thereby reverts mesenchymal and stem cell-like phenotype caused by loss of p53 to differentiated epithelial cell phenotype. Furthermore, loss of p53 negatively correlates with miR-200c level but positively with increased expression of EMT and stemness markers as well as high tumor grade in a cohort of breast tumors. Together, this study elucidates a role of p53 in regulating EMT-MET (mechenchymal epithelial transition) and stemness or differentiation plasticity and reveals a potential therapeutic implication to suppress EMT associated-cancer stem cells through activation of p53-miR-200c pathway. The epithelial to mesenchymal transition (EMT) has been recently associated with a stem cell phenotype. In breast cancer cell lines and tumours, p53 directly targets the expression of microRNAs that have been shown to inhibit EMT and stem cells regulators. The epithelial–mesenchymal transition (EMT) has recently been linked to stem cell phenotype 1 , 2 . However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties 3 , 4 and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT–MET (mesenchymal–epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53–miR-200c pathway. The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype (1,2). However, the molecular mechanism underlying EMT and regulation of stemness remains elusive. Here, using genomic approaches, we show that tumour suppressor p53 has a role in regulating both EMT and EMT-associated stem cell properties through transcriptional activation of the microRNA miR-200c. p53 transactivates miR-200c through direct binding to the miR-200c promoter. Loss of p53 in mammary epithelial cells leads to decreased expression of miR-200c and activates the EMT programme, accompanied by an increased mammary stem cell population. Re-expressing miR-200c suppresses genes that mediate EMT and stemness properties (3,4) and thereby reverts the mesenchymal and stem-cell-like phenotype caused by loss of p53 to a differentiated epithelial cell phenotype. Furthermore, loss of p53 correlates with a decrease in the level of miR-200c, but an increase in the expression of EMT and stemness markers, and development of a high tumour grade in a cohort of breast tumours. This study elucidates a role for p53 in regulating EMT-MET (mesenchymal-epithelial transition) and stemness or differentiation plasticity, and reveals a potential therapeutic implication to suppress EMT-associated cancer stem cells through activation of the p53-miR-200c pathway. |
| Audience | Academic |
| Author | Xiong, Yan Hung, Mien-Chie Liu, Mo Yu, Wen-Hsuan Yang, Jer-Yen Lee, Heng-Huan Yu, Dihua Hsu, Jennifer L. Li, Chia-Wei Xia, Weiya Rehman, Sumaiyah K. Chen, Chun-Te Chang, Chun-Ju Chao, Chi-Hong |
| AuthorAffiliation | 1 Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA 2 Center for Molecular Medicine, China Medical University Hospital; Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan 3 Asian University, Taichung 413, Taiwan |
| AuthorAffiliation_xml | – name: 2 Center for Molecular Medicine, China Medical University Hospital; Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan – name: 3 Asian University, Taichung 413, Taiwan – name: 1 Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA |
| Author_xml | – sequence: 1 givenname: Chun-Ju surname: Chang fullname: Chang, Chun-Ju organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 2 givenname: Chi-Hong surname: Chao fullname: Chao, Chi-Hong organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 3 givenname: Weiya surname: Xia fullname: Xia, Weiya organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 4 givenname: Jer-Yen surname: Yang fullname: Yang, Jer-Yen organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Present address: Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA – sequence: 5 givenname: Yan surname: Xiong fullname: Xiong, Yan organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 6 givenname: Chia-Wei surname: Li fullname: Li, Chia-Wei organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 7 givenname: Wen-Hsuan surname: Yu fullname: Yu, Wen-Hsuan organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 8 givenname: Sumaiyah K. surname: Rehman fullname: Rehman, Sumaiyah K. organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 9 givenname: Jennifer L. surname: Hsu fullname: Hsu, Jennifer L. organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 10 givenname: Heng-Huan surname: Lee fullname: Lee, Heng-Huan organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 11 givenname: Mo surname: Liu fullname: Liu, Mo organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 12 givenname: Chun-Te surname: Chen fullname: Chen, Chun-Te organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 13 givenname: Dihua surname: Yu fullname: Yu, Dihua organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 14 givenname: Mien-Chie surname: Hung fullname: Hung, Mien-Chie email: mhung@mdanderson.org organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Center for Molecular Medicine, China Medical University Hospital; Graduate Institute of Cancer Biology, China Medical University, Graduate Institute of Cancer Biology, China Medical University, Asian University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21336307$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1093/annonc/mdm559 10.1158/1078-0432.CCR-03-0527 10.1128/MCB.00537-06 10.1016/j.cell.2009.07.011 10.1128/MCB.11.1.12 10.1038/ncb1998 10.1038/nrc2620 10.1016/S0378-1119(01)00696-5 10.1172/JCI39194 10.1158/0008-5472.CAN-04-4537 10.1038/nrm1835 10.1016/S0960-9822(00)00002-6 10.1074/jbc.274.39.28042 10.1038/sj.onc.1207396 10.1038/sj.onc.1207947 10.1038/embor.2008.74 10.1016/j.cell.2008.03.027 10.1593/neo.08120 10.1128/JVI.72.11.8463-8471.1998 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 C.-J. Chang and C.-H. Chao contributed equally to this work. Present address: Department of Developmental Biology, Stanford University, Stanford, CA 94305 |
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| References | Xirodimas, Lane (CR20) 1999; 274 Araki (CR11) 2009; 120 Burk (CR15) 2008; 9 Muret (CR19) 2008; 19 Kim, Lee, Bonifant, Ressom, Waldman (CR13) 2007; 27 Wellner (CR4) 2009; 11 Mani (CR1) 2008; 133 Polyak, Weinberg (CR2) 2009; 9 Al-Hajj, Clarke (CR12) 2004; 23 Junk (CR6) 2008; 10 Xia (CR17) 2004; 10 Thiery, Sleeman (CR5) 2006; 7 Nielsen (CR10) 1997; 4 Milner, Medcalf, Cook (CR9) 1991; 11 Cadwell, Zambetti (CR8) 2001; 277 Dull (CR14) 1998; 72 Kramata (CR18) 2005; 65 Jacks (CR16) 1994; 4 Shimono (CR3) 2009; 138 Willis, Jung, Wakefield, Chen (CR7) 2004; 23 K Polyak (BFncb2173_CR2) 2009; 9 SA Mani (BFncb2173_CR1) 2008; 133 DJ Junk (BFncb2173_CR6) 2008; 10 J Muret (BFncb2173_CR19) 2008; 19 S Araki (BFncb2173_CR11) 2009; 120 M Al-Hajj (BFncb2173_CR12) 2004; 23 T Dull (BFncb2173_CR14) 1998; 72 T Jacks (BFncb2173_CR16) 1994; 4 J Milner (BFncb2173_CR9) 1991; 11 P Kramata (BFncb2173_CR18) 2005; 65 U Wellner (BFncb2173_CR4) 2009; 11 LL Nielsen (BFncb2173_CR10) 1997; 4 Y Shimono (BFncb2173_CR3) 2009; 138 JP Thiery (BFncb2173_CR5) 2006; 7 U Burk (BFncb2173_CR15) 2008; 9 DP Xirodimas (BFncb2173_CR20) 1999; 274 JS Kim (BFncb2173_CR13) 2007; 27 W Xia (BFncb2173_CR17) 2004; 10 C Cadwell (BFncb2173_CR8) 2001; 277 A Willis (BFncb2173_CR7) 2004; 23 Nat Cell Biol. 2011 Dec;13(12):1466 Nat Cell Biol. 2011 Dec;13(12):1467 |
| References_xml | – volume: 19 start-page: 793 year: 2008 end-page: 800 ident: CR19 article-title: p53 status correlates with histopathological response in patients with soft tissue sarcomas treated using isolated limb perfusion with TNF-α and melphalan publication-title: Ann. Oncol. doi: 10.1093/annonc/mdm559 – volume: 10 start-page: 3815 year: 2004 end-page: 3824 ident: CR17 article-title: Phosphorylation/cytoplasmic localization of p21Cip1/WAF1 is associated with HER2/neu overexpression and provides a novel combination predictor for poor prognosis in breast cancer patients publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-03-0527 – volume: 27 start-page: 662 year: 2007 end-page: 677 ident: CR13 article-title: Activation of p53-dependent growth suppression in human cells by mutations in or publication-title: Mol. Cell Biol. doi: 10.1128/MCB.00537-06 – volume: 138 start-page: 592 year: 2009 end-page: 603 ident: CR3 article-title: Downregulation of miRNA-200c links breast cancer stem cells with normal stem cells publication-title: Cell doi: 10.1016/j.cell.2009.07.011 – volume: 11 start-page: 12 year: 1991 end-page: 19 ident: CR9 article-title: Tumor suppressor p53: analysis of wild-type and mutant p53 complexes publication-title: Mol. Cell Biol. doi: 10.1128/MCB.11.1.12 – volume: 11 start-page: 1487 year: 2009 end-page: 1495 ident: CR4 article-title: The EMT-activator ZEB1 promotes tumorigenicity by repressing stemness-inhibiting microRNAs publication-title: Nat. Cell Biol. doi: 10.1038/ncb1998 – volume: 9 start-page: 265 year: 2009 end-page: 273 ident: CR2 article-title: Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits publication-title: Nat. Rev. Cancer doi: 10.1038/nrc2620 – volume: 277 start-page: 15 year: 2001 end-page: 30 ident: CR8 article-title: The effects of wild-type p53 tumor suppressor activity and mutant p53 gain-of-function on cell growth publication-title: Gene doi: 10.1016/S0378-1119(01)00696-5 – volume: 120 start-page: 290 year: 2009 end-page: 302 ident: CR11 article-title: TGF-β1-induced expression of human Mdm2 correlates with late-stage metastatic breast cancer publication-title: J. Clin. Invest. doi: 10.1172/JCI39194 – volume: 65 start-page: 3577 year: 2005 end-page: 3585 ident: CR18 article-title: Patches of mutant p53-immunoreactive epidermal cells induced by chronic UVB irradiation harbor the same p53 mutations as squamous cell carcinomas in the skin of hairless SKH-1 mice publication-title: Cancer Res. doi: 10.1158/0008-5472.CAN-04-4537 – volume: 7 start-page: 131 year: 2006 end-page: 142 ident: CR5 article-title: Complex networks orchestrate epithelial–mesenchymal transitions publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm1835 – volume: 4 start-page: 1 year: 1994 end-page: 7 ident: CR16 article-title: Tumor spectrum analysis in p53-mutant mice publication-title: Curr. Biol. doi: 10.1016/S0960-9822(00)00002-6 – volume: 274 start-page: 28042 year: 1999 end-page: 28049 ident: CR20 article-title: Molecular evolution of the thermosensitive PAb1620 epitope of human p53 by DNA shuffling publication-title: J. Biol. Chem. doi: 10.1074/jbc.274.39.28042 – volume: 23 start-page: 2330 year: 2004 end-page: 2338 ident: CR7 article-title: Mutant p53 exerts a dominant negative effect by preventing wild-type p53 from binding to the promoter of its target genes publication-title: Oncogene doi: 10.1038/sj.onc.1207396 – volume: 4 start-page: 129 year: 1997 end-page: 138 ident: CR10 article-title: Efficacy of p53 adenovirus-mediated gene therapy against human breast cancer xenografts publication-title: Cancer Gene Ther. – volume: 23 start-page: 7274 year: 2004 end-page: 7282 ident: CR12 article-title: Self-renewal and solid tumor stem cells publication-title: Oncogene doi: 10.1038/sj.onc.1207947 – volume: 72 start-page: 8463 year: 1998 end-page: 8471 ident: CR14 article-title: A third-generation lentivirus vector with a conditional packaging system publication-title: J. Virol. – volume: 9 start-page: 582 year: 2008 end-page: 589 ident: CR15 article-title: A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells publication-title: EMBO Rep. doi: 10.1038/embor.2008.74 – volume: 133 start-page: 704 year: 2008 end-page: 715 ident: CR1 article-title: The epithelial–mesenchymal transition generates cells with properties of stem cells publication-title: Cell doi: 10.1016/j.cell.2008.03.027 – volume: 10 start-page: 450 year: 2008 end-page: 461 ident: CR6 article-title: Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cells publication-title: Neoplasia doi: 10.1593/neo.08120 – volume: 65 start-page: 3577 year: 2005 ident: BFncb2173_CR18 publication-title: Cancer Res. doi: 10.1158/0008-5472.CAN-04-4537 – volume: 4 start-page: 1 year: 1994 ident: BFncb2173_CR16 publication-title: Curr. Biol. doi: 10.1016/S0960-9822(00)00002-6 – volume: 27 start-page: 662 year: 2007 ident: BFncb2173_CR13 publication-title: Mol. Cell Biol. doi: 10.1128/MCB.00537-06 – volume: 9 start-page: 582 year: 2008 ident: BFncb2173_CR15 publication-title: EMBO Rep. doi: 10.1038/embor.2008.74 – volume: 120 start-page: 290 year: 2009 ident: BFncb2173_CR11 publication-title: J. Clin. Invest. doi: 10.1172/JCI39194 – volume: 133 start-page: 704 year: 2008 ident: BFncb2173_CR1 publication-title: Cell doi: 10.1016/j.cell.2008.03.027 – volume: 10 start-page: 3815 year: 2004 ident: BFncb2173_CR17 publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-03-0527 – volume: 9 start-page: 265 year: 2009 ident: BFncb2173_CR2 publication-title: Nat. Rev. Cancer doi: 10.1038/nrc2620 – volume: 11 start-page: 1487 year: 2009 ident: BFncb2173_CR4 publication-title: Nat. Cell Biol. doi: 10.1038/ncb1998 – volume: 23 start-page: 7274 year: 2004 ident: BFncb2173_CR12 publication-title: Oncogene doi: 10.1038/sj.onc.1207947 – volume: 11 start-page: 12 year: 1991 ident: BFncb2173_CR9 publication-title: Mol. Cell Biol. doi: 10.1128/MCB.11.1.12 – volume: 23 start-page: 2330 year: 2004 ident: BFncb2173_CR7 publication-title: Oncogene doi: 10.1038/sj.onc.1207396 – volume: 19 start-page: 793 year: 2008 ident: BFncb2173_CR19 publication-title: Ann. Oncol. doi: 10.1093/annonc/mdm559 – volume: 274 start-page: 28042 year: 1999 ident: BFncb2173_CR20 publication-title: J. Biol. Chem. doi: 10.1074/jbc.274.39.28042 – volume: 138 start-page: 592 year: 2009 ident: BFncb2173_CR3 publication-title: Cell doi: 10.1016/j.cell.2009.07.011 – volume: 277 start-page: 15 year: 2001 ident: BFncb2173_CR8 publication-title: Gene doi: 10.1016/S0378-1119(01)00696-5 – volume: 4 start-page: 129 year: 1997 ident: BFncb2173_CR10 publication-title: Cancer Gene Ther. – volume: 72 start-page: 8463 year: 1998 ident: BFncb2173_CR14 publication-title: J. Virol. doi: 10.1128/JVI.72.11.8463-8471.1998 – volume: 10 start-page: 450 year: 2008 ident: BFncb2173_CR6 publication-title: Neoplasia doi: 10.1593/neo.08120 – volume: 7 start-page: 131 year: 2006 ident: BFncb2173_CR5 publication-title: Nat. Rev. Mol. Cell Biol. doi: 10.1038/nrm1835 – reference: - Nat Cell Biol. 2011 Dec;13(12):1467 – reference: - Nat Cell Biol. 2011 Dec;13(12):1466 |
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| Snippet | The epithelial to mesenchymal transition (EMT) has been recently associated with a stem cell phenotype. In breast cancer cell lines and tumours, p53 directly... The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype. However, the molecular mechanism underlying EMT and regulation of... The epithelial-mesenchymal transition (EMT) has recently been linked to stem cell phenotype (1,2). However, the molecular mechanism underlying EMT and... Epithelial mechenchymal transition (EMT) has recently been linked to stem cell phenotype 1 , 2 . However, the molecular mechanism involving regulation of EMT... |
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| SubjectTerms | 631/136/532 631/208/200 631/80/84/2176 Aneuploidy Biology Biomedical and Life Sciences Breast Neoplasms - metabolism Cancer Cancer Research Cell Biology Cell Line, Tumor Cell Lineage Cytokinesis Developmental Biology Entosis Epithelial-Mesenchymal Transition Gene Expression Regulation, Neoplastic Genes, p53 Genotype & phenotype Humans letter Life Sciences MicroRNA MicroRNAs MicroRNAs - genetics Microscopy, Fluorescence - methods Mitosis Physiological aspects Plasticity Stem Cells Stem Cells - cytology Tumor suppressor genes Tumor Suppressor Protein p53 - metabolism Tumors |
| Title | p53 regulates epithelial–mesenchymal transition and stem cell properties through modulating miRNAs |
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