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  • 1
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    Generation of a prostate from a single adult stem cell (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-24
    Description: The existence of prostate stem cells (PSCs) was first postulated from the observation that normal prostate regeneration can occur after repeated cycles of androgen deprivation and replacement in rodents. Given the critical role of PSCs in maintaining prostate tissue integrity and their potential involvement in prostate tumorigenesis, it is important to define specific markers for normal PSCs. Several cell-surface markers have been reported to identify candidate PSCs, including stem cell antigen-1 (Sca-1, also known as Ly6a), CD133 (Prom1) and CD44 (refs 3-10). However, many non-PSCs in the mouse prostate also express these markers and thus identification of a more defined PSC population remains elusive. Here we identify CD117 (c-kit, stem cell factor receptor) as a new marker of a rare adult mouse PSC population, and demonstrate that a single stem cell defined by the phenotype Lin(-)Sca-1(+)CD133(+)CD44(+)CD117(+) can generate a prostate after transplantation in vivo. CD117 expression is predominantly localized to the region of the mouse prostate proximal to the urethra and is upregulated after castration-induced prostate involution-two characteristics consistent with that of a PSC marker. CD117(+) PSCs can generate functional, secretion-producing prostates when transplanted in vivo. Moreover, CD117(+) PSCs have long-term self-renewal capacity, as evidenced by serial isolation and transplantation in vivo. Our data establish that single cells in the adult mouse prostate with multipotent, self-renewal capacity are defined by a Lin(-)Sca-1(+)CD133(+)CD44(+)CD117(+) phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leong, Kevin G -- Wang, Bu-Er -- Johnson, Leisa -- Gao, Wei-Qiang -- England -- Nature. 2008 Dec 11;456(7223):804-8. doi: 10.1038/nature07427. Epub 2008 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18946470" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/metabolism/*physiology/*transplantation ; Animals ; Antigens, Surface/genetics ; Epithelium/metabolism ; Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; Phenotype ; Prostate/*cytology/*growth & development/metabolism/secretion ; Proto-Oncogene Proteins c-kit/genetics ; *Stem Cell Transplantation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    COP1 is a tumour suppressor that causes degradation of ETS transcription factors (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-05-17
    Description: The proto-oncogenes ETV1, ETV4 and ETV5 encode transcription factors in the E26 transformation-specific (ETS) family, which includes the most frequently rearranged and overexpressed genes in prostate cancer. Despite being critical regulators of development, little is known about their post-translational regulation. Here we identify the ubiquitin ligase COP1 (also known as RFWD2) as a tumour suppressor that negatively regulates ETV1, ETV4 and ETV5. ETV1, which is mutated in prostate cancer more often, was degraded after being ubiquitinated by COP1. Truncated ETV1 encoded by prostate cancer translocation TMPRSS2:ETV1 lacks the critical COP1 binding motifs and was 50-fold more stable than wild-type ETV1. Almost all patient translocations render ETV1 insensitive to COP1, implying that this confers a selective advantage to prostate epithelial cells. Indeed, COP1 deficiency in mouse prostate elevated ETV1 and produced increased cell proliferation, hyperplasia, and early prostate intraepithelial neoplasia. Combined loss of COP1 and PTEN enhanced the invasiveness of mouse prostate adenocarcinomas. Finally, rare human prostate cancer samples showed hemizygous loss of the COP1 gene, loss of COP1 protein, and elevated ETV1 protein while lacking a translocation event. These findings identify COP1 as a tumour suppressor whose downregulation promotes prostatic epithelial cell proliferation and tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitari, Alberto C -- Leong, Kevin G -- Newton, Kim -- Yee, Cindy -- O'Rourke, Karen -- Liu, Jinfeng -- Phu, Lilian -- Vij, Rajesh -- Ferrando, Ronald -- Couto, Suzana S -- Mohan, Sankar -- Pandita, Ajay -- Hongo, Jo-Anne -- Arnott, David -- Wertz, Ingrid E -- Gao, Wei-Qiang -- French, Dorothy M -- Dixit, Vishva M -- England -- Nature. 2011 May 15;474(7351):403-6. doi: 10.1038/nature10005.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiological Chemistry, Genentech, Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21572435" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Carrier Proteins/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; DNA-Binding Proteins/genetics/metabolism ; Humans ; Male ; Mice ; Nuclear Proteins/deficiency/*metabolism ; PTEN Phosphohydrolase/deficiency ; Prostatic Neoplasms/metabolism/pathology ; Protein Binding ; Proto-Oncogene Proteins c-ets/*metabolism ; Transcription Factors/genetics/metabolism ; Tumor Suppressor Proteins/*metabolism ; Ubiquitin-Protein Ligases/deficiency/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Sensitivity to antitubulin chemotherapeutics is regulated by MCL1 and FBW7 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-04
    Description: Microtubules have pivotal roles in fundamental cellular processes and are targets of antitubulin chemotherapeutics. Microtubule-targeted agents such as Taxol and vincristine are prescribed widely for various malignancies, including ovarian and breast adenocarcinomas, non-small-cell lung cancer, leukaemias and lymphomas. These agents arrest cells in mitosis and subsequently induce cell death through poorly defined mechanisms. The strategies that resistant tumour cells use to evade death induced by antitubulin agents are also unclear. Here we show that the pro-survival protein MCL1 (ref. 3) is a crucial regulator of apoptosis triggered by antitubulin chemotherapeutics. During mitotic arrest, MCL1 protein levels decline markedly, through a post-translational mechanism, potentiating cell death. Phosphorylation of MCL1 directs its interaction with the tumour-suppressor protein FBW7, which is the substrate-binding component of a ubiquitin ligase complex. The polyubiquitylation of MCL1 then targets it for proteasomal degradation. The degradation of MCL1 was blocked in patient-derived tumour cells that lacked FBW7 or had loss-of-function mutations in FBW7, conferring resistance to antitubulin agents and promoting chemotherapeutic-induced polyploidy. Additionally, primary tumour samples were enriched for FBW7 inactivation and elevated MCL1 levels, underscoring the prominent roles of these proteins in oncogenesis. Our findings suggest that profiling the FBW7 and MCL1 status of tumours, in terms of protein levels, messenger RNA levels and genetic status, could be useful to predict the response of patients to antitubulin chemotherapeutics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wertz, Ingrid E -- Kusam, Saritha -- Lam, Cynthia -- Okamoto, Toru -- Sandoval, Wendy -- Anderson, Daniel J -- Helgason, Elizabeth -- Ernst, James A -- Eby, Mike -- Liu, Jinfeng -- Belmont, Lisa D -- Kaminker, Josh S -- O'Rourke, Karen M -- Pujara, Kanan -- Kohli, Pawan Bir -- Johnson, Adam R -- Chiu, Mark L -- Lill, Jennie R -- Jackson, Peter K -- Fairbrother, Wayne J -- Seshagiri, Somasekar -- Ludlam, Mary J C -- Leong, Kevin G -- Dueber, Erin C -- Maecker, Heather -- Huang, David C S -- Dixit, Vishva M -- CA043540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- England -- Nature. 2011 Mar 3;471(7336):110-4. doi: 10.1038/nature09779.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Early Discovery Biochemistry, Genentech, South San Francisco, California 94080, USA. ingrid@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21368834" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Cell Cycle Proteins/genetics/*metabolism ; Cell Line ; Cell Line, Tumor ; Cell Transformation, Neoplastic/drug effects ; Drug Resistance, Neoplasm ; F-Box Proteins/genetics/*metabolism ; Fibroblasts ; Humans ; Mice ; Mitosis/drug effects ; Myeloid Cell Leukemia Sequence 1 Protein ; Paclitaxel/pharmacology ; Pharmacogenetics ; Phosphorylation/drug effects ; Polyploidy ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding/drug effects ; Proto-Oncogene Proteins c-bcl-2/deficiency/genetics/*metabolism ; RNA, Messenger/genetics/metabolism ; Tubulin/*metabolism ; Tubulin Modulators/*pharmacology ; Ubiquitin-Protein Ligases/deficiency/genetics/*metabolism ; Vincristine/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    A reserve stem cell population in small intestine renders Lgr5-positive cells dispensable (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-09-20
    Description: The small intestine epithelium renews every 2 to 5 days, making it one of the most regenerative mammalian tissues. Genetic inducible fate mapping studies have identified two principal epithelial stem cell pools in this tissue. One pool consists of columnar Lgr5-expressing cells that cycle rapidly and are present predominantly at the crypt base. The other pool consists of Bmi1-expressing cells that largely reside above the crypt base. However, the relative functions of these two pools and their interrelationship are not understood. Here we specifically ablated Lgr5-expressing cells in mice using a human diphtheria toxin receptor (DTR) gene knocked into the Lgr5 locus. We found that complete loss of the Lgr5-expressing cells did not perturb homeostasis of the epithelium, indicating that other cell types can compensate for the elimination of this population. After ablation of Lgr5-expressing cells, progeny production by Bmi1-expressing cells increased, indicating that Bmi1-expressing stem cells compensate for the loss of Lgr5-expressing cells. Indeed, lineage tracing showed that Bmi1-expressing cells gave rise to Lgr5-expressing cells, pointing to a hierarchy of stem cells in the intestinal epithelium. Our results demonstrate that Lgr5-expressing cells are dispensable for normal intestinal homeostasis, and that in the absence of these cells, Bmi1-expressing cells can serve as an alternative stem cell pool. These data provide the first experimental evidence for the interrelationship between these populations. The Bmi1-expressing stem cells may represent both a reserve stem cell pool in case of injury to the small intestine epithelium and a source for replenishment of the Lgr5-expressing cells under non-pathological conditions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4251967/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4251967/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tian, Hua -- Biehs, Brian -- Warming, Soren -- Leong, Kevin G -- Rangell, Linda -- Klein, Ophir D -- de Sauvage, Frederic J -- 1-DP2-OD007191/OD/NIH HHS/ -- DP2 OD007191/OD/NIH HHS/ -- R01 DE021420/DE/NIDCR NIH HHS/ -- R01-DE021420/DE/NIDCR NIH HHS/ -- England -- Nature. 2011 Sep 18;478(7368):255-9. doi: 10.1038/nature10408.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21927002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Epithelial Cells/cytology/metabolism ; Female ; Heparin-binding EGF-like Growth Factor ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/genetics/metabolism ; Intestine, Small/*cytology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*metabolism ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins/*metabolism ; Receptors, G-Protein-Coupled/deficiency/genetics/*metabolism ; Regeneration ; Repressor Proteins/*metabolism ; Stem Cells/*cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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