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  • 1
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    Online Resource
    Rb1 and Trp53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance
    American Association for the Advancement of Science (AAAS) ; 2017
    In:  Science Vol. 355, No. 6320 ( 2017-01-06), p. 78-83
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 355, No. 6320 ( 2017-01-06), p. 78-83
    Abstract: Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting that lineage plasticity facilitates therapeutic resistance. The mechanisms underlying prostate cancer lineage plasticity are incompletely understood. Studying mouse models, we demonstrate that Rb1 loss facilitates lineage plasticity and metastasis of prostate adenocarcinoma initiated by Pten mutation. Additional loss of Trp53 causes resistance to antiandrogen therapy. Gene expression profiling indicates that mouse tumors resemble human prostate cancer neuroendocrine variants; both mouse and human tumors exhibit increased expression of epigenetic reprogramming factors such as Ezh2 and Sox2. Clinically relevant Ezh2 inhibitors restore androgen receptor expression and sensitivity to antiandrogen therapy. These findings uncover genetic mutations that enable prostate cancer progression; identify mouse models for studying prostate cancer lineage plasticity; and suggest an epigenetic approach for extending clinical responses to antiandrogen therapy.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aah4199
    RVK:
    TA 1000
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2017
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  • 2
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    The THO Ribonucleoprotein Complex Is Required for Stem Cell Homeostasis in the Adult Mouse Small Intestine
    Informa UK Limited ; 2013
    In:  Molecular and Cellular Biology Vol. 33, No. 17 ( 2013-09-01), p. 3505-3514
    Details
    In: Molecular and Cellular Biology, Informa UK Limited, Vol. 33, No. 17 ( 2013-09-01), p. 3505-3514
    Type of Medium: Online Resource
    ISSN: 1098-5549
    URL: Article
    DOI: 10.1128/MCB.00751-13
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2013
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  • 3
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    Abstract B24: Thoc1 is required for mouse prostate tumorigenesis initiated by loss of Rb and p53
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Research Vol. 69, No. 23_Supplement ( 2009-12-01), p. B24-B24
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 69, No. 23_Supplement ( 2009-12-01), p. B24-B24
    Abstract: A large percentage of prostate cancers show either mutational inactivation or deregulation of the Rb tumor suppressor gene. Rb mediates its tumor suppressor function through its association with other cellular proteins. Most of the Rb-binding proteins interact with the A/B pocket domain and the C terminal region. Less than 10 proteins are known to interact with Rb N terminal domain, a domain that appears to be required for normal Rb function in vivo. The Thoc1 gene encodes a protein that binds the Rb N terminal domain. We hypothesize that some of pRb functions in vivo could be mediated in part by interaction with pThoc1. Thoc1 protein has been found to be an essential component of the TREX (transcription/export) complex which is important for mRNP biogenesis and physically couples transcription elongation with RNA processing and export. We have previously reported that E1A/Ras transformed MEFs (mouse embryonic fibroblasts) but not normal MEFs were dependent on Thoc1 for their survival. These observations suggest that tumor cells specifically may be dependent on Thoc1 for survival and Thoc1 may play a role in tumorigenesis. To test our hypothesis, we used a mouse model of prostate cancer where prostatespecific deletion of Rb and p53 genes leads to development of metastatic adenocarcinoma. We find that compound loss of Thoc1, Rb and p53 increased the life-span of mice compared to mice with loss of Rb and p53 alone. Histopathological analyses of prostate tissue showed that initiation of tumorigenesis is delayed in the absence of Thoc1. Tumors that do arise in these mice retain expression of Thoc1. These findings indicate that Thoc1 is required for prostate tumorigenesis. Conditional deletion of Thoc1 alone in mouse prostate does not appear to affect normal prostate development. To test whether Thoc1 is relevant to human prostate cancer, we examined expression of Thoc1 protein in matched normal and prostate tumor tissue cores on tissue microarray. Analysis of nearly 600 patient samples reveals that Thoc1 is significantly overexpressed in tumor tissue compared to normal prostate tissue and pThoc1 levels positively correlated with tumor grade and negatively correlated with biochemical recurrence as indicated by elevated PSA (prostate-specific antigen) levels. Taken together the above findings suggest that Thoc1 is synthetic lethal with the genetic and epigenetic alterations in prostate tumor cells, and hence it may be a potential target for prostate cancer therapy. Citation Information: Cancer Res 2009;69(23 Suppl):B24.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.FBCR09-B24
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
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  • 4
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    E2f binding-deficient Rb1 protein suppresses prostate tumor progression in vivo
    Proceedings of the National Academy of Sciences ; 2011
    In:  Proceedings of the National Academy of Sciences Vol. 108, No. 2 ( 2011-01-11), p. 704-709
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 108, No. 2 ( 2011-01-11), p. 704-709
    Abstract: Mutational inactivation of the RB1 tumor suppressor gene initiates retinoblastoma and other human cancers. RB1 protein (pRb) restrains cell proliferation by binding E2f transcription factors and repressing the expression of cell cycle target genes. It is presumed that loss of pRb/E2f interaction accounts for tumor initiation, but this has not been directly tested. RB1 mutation is a late event in other human cancers, suggesting a role in tumor progression as well as initiation. It is currently unknown whether RB1 mutation drives tumor progression and, if so, whether loss of pRb/E2f interaction is responsible. We have characterized tumorigenesis in mice expressing a mutant pRb that is specifically deficient in binding E2f. In endocrine tissue, the mutant pRb has no detectable effect on tumorigenesis. In contrast, it significantly delays progression to invasive and lethal prostate cancer. Tumor delay is associated with induction of a senescence response. We conclude that the pRb/E2f interaction is critical for preventing tumor initiation, but that pRb can use additional context-dependent mechanisms to restrain tumor progression.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1015027108
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2011
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  • 5
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    Cancer Cells and Normal Cells Differ in Their Requirements for Thoc1
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 14 ( 2007-07-15), p. 6657-6664
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 14 ( 2007-07-15), p. 6657-6664
    Abstract: The evolutionarily conserved TREX (Transcription/Export) complex physically couples transcription, messenger ribonucleoprotein particle biogenesis, RNA processing, and RNA export for a subset of genes. HPR1 encodes an essential component of the S. cerevisiae TREX complex. HPR1 loss compromises transcriptional elongation, nuclear RNA export, and genome stability. Yet, HPR1 is not required for yeast viability. Thoc1 is the recently discovered human functional orthologue of HPR1. Thoc1 is expressed at higher levels in breast cancer than in normal epithelia, and expression levels correlate with tumor size and metastatic potential. Depletion of Thoc1 protein (pThoc1) in human cancer cell lines compromises cell proliferation. It is currently unclear whether Thoc1 is essential for all mammalian cells or whether cancer cells may differ from normal cells in their dependence on Thoc1. To address this issue, we have compared the requirements for Thoc1 in the proliferation and survival of isogenic normal and oncogene-transformed cells. Neoplastic cells rapidly lose viability via apoptotic cell death on depletion of pThoc1. Induction of apoptotic cell death is coincident with increased DNA damage as indicated by the appearance of phosphorylated histone H2AX. In contrast, the viability of normal cells is largely unaffected by pThoc1 loss. Normal cells lacking Thoc1 cannot be transformed by forced expression of E1A and Ha-ras, suggesting that Thoc1 may be important for neoplastic transformation. In sum, our data are consistent with the hypothesis that cancer cells require higher levels of pThoc1 for survival than normal cells. If true, pThoc1 may provide a novel molecular target for cancer therapy. [Cancer Res 2007;67(14):6657–64]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-06-3234
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
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  • 6
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    MDM2 E3 ligase activity is essential for p53 regulation and cell cycle integrity
    Public Library of Science (PLoS) ; 2022
    In:  PLOS Genetics Vol. 18, No. 5 ( 2022-5-19), p. e1010171-
    Details
    In: PLOS Genetics, Public Library of Science (PLoS), Vol. 18, No. 5 ( 2022-5-19), p. e1010171-
    Abstract: MDM2 and MDM4 are key regulators of p53 and function as oncogenes when aberrantly expressed. MDM2 and MDM4 partner to suppress p53 transcriptional transactivation and polyubiquitinate p53 for degradation. The importance of MDM2 E3-ligase-mediated p53 regulation remains controversial. To resolve this, we generated mice with an Mdm2 L466A mutation that specifically compromises E2 interaction, abolishing MDM2 E3 ligase activity while preserving its ability to bind MDM4 and suppress p53 transactivation. Mdm2 L466A/L466A mice exhibit p53-dependent embryonic lethality, demonstrating MDM2 E3 ligase activity is essential for p53 regulation in vivo . Unexpectedly, cells expressing Mdm2 L466A manifest cell cycle G2-M transition defects and increased aneuploidy even in the absence of p53, suggesting MDM2 E3 ligase plays a p53-independent role in cell cycle regulation and genome integrity. Furthermore, cells bearing the E3-dead MDM2 mutant show aberrant cell cycle regulation in response to DNA damage. This study uncovers an uncharacterized role for MDM2’s E3 ligase activity in cell cycle beyond its essential role in regulating p53’s stability in vivo .
    Type of Medium: Online Resource
    ISSN: 1553-7404
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    DOI: 10.1371/journal.pgen.1010171
    DOI: 10.1371/journal.pgen.1010171.g001
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    DOI: 10.1371/journal.pgen.1010171.g007
    DOI: 10.1371/journal.pgen.1010171.t001
    DOI: 10.1371/journal.pgen.1010171.s001
    DOI: 10.1371/journal.pgen.1010171.s002
    DOI: 10.1371/journal.pgen.1010171.s003
    DOI: 10.1371/journal.pgen.1010171.s004
    DOI: 10.1371/journal.pgen.1010171.s005
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    DOI: 10.1371/journal.pgen.1010171.s007
    DOI: 10.1371/journal.pgen.1010171.s008
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2022
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  • 7
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    Differential expression of αVβ3 and αVβ6 integrins in prostate cancer progression
    Public Library of Science (PLoS) ; 2021
    In:  PLOS ONE Vol. 16, No. 1 ( 2021-1-22), p. e0244985-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 16, No. 1 ( 2021-1-22), p. e0244985-
    Abstract: Neuroendocrine prostate cancer (NEPrCa) arises de novo or after accumulation of genomic alterations in pre-existing adenocarcinoma tumors in response to androgen deprivation therapies. We have provided evidence that small extracellular vesicles released by PrCa cells and containing the αVβ3 integrin promote neuroendocrine differentiation of PrCa in vivo and in vitro . Here, we examined αVβ3 integrin expression in three murine models carrying a deletion of PTEN (SKO), PTEN and RB1 (DKO), or PTEN , RB1 and TRP53 (TKO) genes in the prostatic epithelium; of these three models, the DKO and TKO tumors develop NEPrCa with a gene signature comparable to those of human NEPrCa. Immunostaining analysis of SKO, DKO and TKO tumors shows that αVβ3 integrin expression is increased in DKO and TKO primary tumors and metastatic lesions, but absent in SKO primary tumors. On the other hand, SKO tumors show higher levels of a different αV integrin, αVβ6, as compared to DKO and TKO tumors. These results are confirmed by RNA-sequencing analysis. Moreover, TRAMP mice, which carry NEPrCa and adenocarcinoma of the prostate, also have increased levels of αVβ3 in their NEPrCa primary tumors. In contrast, the αVβ6 integrin is only detectable in the adenocarcinoma areas. Finally, analysis of 42 LuCaP patient-derived xenografts and primary adenocarcinoma samples shows a positive correlation between αVβ3, but not αVβ6, and the neuronal marker synaptophysin; it also demonstrates that αVβ3 is absent in prostatic adenocarcinomas. In summary, we demonstrate that αVβ3 integrin is upregulated in NEPrCa primary and metastatic lesions; in contrast, the αVβ6 integrin is confined to adenocarcinoma of the prostate. Our findings suggest that the αVβ3 integrin, but not αVβ6, may promote a shift in lineage plasticity towards a NE phenotype and might serve as an informative biomarker for the early detection of NE differentiation in prostate cancer.
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
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    DOI: 10.1371/journal.pone.0244985
    DOI: 10.1371/journal.pone.0244985.g001
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    DOI: 10.1371/journal.pone.0244985.t001
    DOI: 10.1371/journal.pone.0244985.s001
    DOI: 10.1371/journal.pone.0244985.s002
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2021
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  • 8
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    Abstract 2606: Requirement of MDM2 E3 ligase activity for regulating p53 during normal development, cell cycle regulation and genome integrity
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2606-2606
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2606-2606
    Abstract: p53 tumor suppressor, the most mutated gene in human cancer, is negatively regulated by MDM2 and MDM4 proteins. Two distinct mechanisms of MDM2/MDM4 regulation of p53 include, one, suppression of p53 transactivation activity by direct interaction of MDM2/MDM4 with p53 protein, thus blocking its transactivation interface and two, targeting p53 to proteasomal degradation by MDM2 E3 ligase activity. However, the importance of these mechanisms in normal p53 regulation in vivo has remained controversial. To genetically separate these two mechanisms of p53 regulation we generated a novel Mdm2 mutant mouse (Mdm2L466A) that lacks E3 ligase activity but retains the ability of Mdm2 to heterodimerize with Mdm4 and inhibit p53 transactivation. Homozygous Mdm2L466A mice are embryonic lethal due to dysregulated p53 activity, thus demonstrating Mdm2 E3 ligase mediated regulation of p53 is essential during embryonic development. Additionally, we uncovered novel p53-independent functions of MDM2 E3 ligase in cell cycle regulation and genome integrity in cells. Cells lacking MDM2 E3 ligase activity have defective G2-M transition during cell cycle and developed elevated levels of aneuploidy regardless of p53 status. This study unequivocally demonstrates the requirement of Mdm2 E3 ligase activity for normal regulation of p53 and uncovers previously unknown p53-independent role of Mdm2 in cell cycle regulation and maintaining genome integrity. A current therapeutic approach involves blocking MDM2-p53 interaction to promote p53 tumor suppression function in cancer cells. Our findings suggest that this approach alone is insufficient because MDM2 has other potential oncogenic mechanisms independent of its role as negative regulator of p53. Hence, targeting MDM2 E3 ligase activity is likely to be more effective cancer therapy as it addresses both p53-dependent and p53-independent oncogenic mechanisms of MDM2. Citation Format: Meenalakshmi Chinnam, Rati Lama, Chao Xu, Xiaojing Zhang, Carlos Cedeno, Yanqing Wang, Aimee B. Stablewski, David W. Goodrich, Xinjiang Wang. Requirement of MDM2 E3 ligase activity for regulating p53 during normal development, cell cycle regulation and genome integrity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2606.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-2606
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 9
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    Abstract LB-143: The role of Thoc1 in cell differentiation of the small intestine
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-143-LB-143
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. LB-143-LB-143
    Abstract: Thoc1 encodes an RNA binding protein (pThoc1) that was identified due to its interaction with the retinoblastoma tumor suppressor protein (Rb). pThoc1 regulates transcriptional elongation and mRNA export as part of the TREX/THO (Transcription/Export) complex. In vivo, mice lacking Thoc1 fail to develop past the late blastocyst stage and mice hypomorphic for Thoc1 have compromised gametogenesis and are sterile. Elevated levels of pThoc1 occur in multiple cancers (breast, lung, colorectal), in cancer cell lines, and in transformed fibroblasts. In vitro, neoplastic cells appear to be more sensitive to pThoc1 loss than normal cells. These observations lead to the hypothesis that cells with extended replicative potential (i.e. stem, progenitor, & cancer cells) require Thoc1. To test this hypothesis, we are examining the role of Thoc1 in vivo utilizing the crypt-villus axis of the murine small intestine as a model system. We have deleted Thoc1 in the murine small intestine using the Rosa26CreER transgene and the Tamoxifen induced CreER mediated recombination system. Thoc1F/F:Rosa26CreER (test) and Thoc1+/+:Rosa26CreER (control) 22 week old mice were treated with intraperitoneal injections of 1mg/day Tamoxifen for 5 days. Small intestinal tissue was collected 24 hours after the last injection. Histological analysis shows Thoc1 deletion disrupts small intestinal crypt architecture, but does not affect villus architecture. Immunohistochemistry illustrates Thoc1 deletion correlates with an increase in cleaved Caspase 3 and decrease in Ki67 in the crypts. No cleaved Caspase 3 is observed in the differentiated villi. These findings suggest intestinal stem cells (ISCs) and progenitor transit amplifying cells of the highly proliferative intestinal crypts require Thoc1 to a greater extent than the differentiated cells of the villi. Since the presence of Thoc1 appears to be required in the crypts, we investigated how Tamoxifen treatment and Thoc1 deletion would affect the crypt-villus axis over time. Thoc1F/F:Rosa26CreER and Thoc1+/+:Rosa26CreER mice were treated as previously described, however small intestinal tissue was collected 3 weeks after the last Tamoxifen injection. Interestingly, no change in body weight, survival, or crypt-villus architecture was observed. These findings lead us to believe ISCs lacking Thoc1 are at a competitive disadvantage and will eventually be replaced by Thoc1 positive ISCs. Consistent with this, while Thoc1 deletion and pThoc1 loss was readily detected 24 hours after Tamoxifen treatment, it was not three weeks after treatment. Future work involves deleting Thoc1 specifically in ISCs using the Lgr5CreER transgene to allow cell differentiation lineage tracing and cell fate studies of ISCs in which Thoc1 has been deleted. Additionally, since Thoc1 is elevated in multiple tumor types, we will delete Thoc1 in transformed ISCs using the Lgr5CreER transgene in ApcMin/+ mice to study Thoc1 in cancer stem cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-143. doi:10.1158/1538-7445.AM2011-LB-143
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-LB-143
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 10
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    Generation of Tumor Organoids from Genetically Engineered Mouse Models of Prostate Cancer
    MyJove Corporation ; 2019
    In:  Journal of Visualized Experiments , No. 148 ( 2019-06-13)
    Details
    In: Journal of Visualized Experiments, MyJove Corporation, , No. 148 ( 2019-06-13)
    Type of Medium: Online Resource
    ISSN: 1940-087X
    URL: Article
    DOI: 10.3791/59710-v
    Language: English
    Publisher: MyJove Corporation
    Publication Date: 2019
    detail.hit.zdb_id: 2259946-0
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