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  1. Article: Chromatin structure and 3D architecture define differential functions of

    Qiu, Kevin / Vu, Duc / Wang, Leran / Bookstaver, Anna / Dinh, Thang N / Goldfarb, Adam N / Tenen, Daniel G / Trinh, Bon Q

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The precise spatio-temporal expression of the hematopoietic ETS transcription ... ...

    Abstract The precise spatio-temporal expression of the hematopoietic ETS transcription factor
    Language English
    Publishing date 2024-01-01
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.01.573782
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: PU.1-c-Jun interaction is crucial for PU.1 function in myeloid development.

    Zhao, Xinhui / Bartholdy, Boris / Yamamoto, Yukiya / Evans, Erica K / Alberich-Jordà, Meritxell / Staber, Philipp B / Benoukraf, Touati / Zhang, Pu / Zhang, Junyan / Trinh, Bon Q / Crispino, John D / Hoang, Trang / Bassal, Mahmoud A / Tenen, Daniel G

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 961

    Abstract: The Ets transcription factor PU.1 is essential for inducing the differentiation of monocytes, macrophages, and B cells in fetal liver and adult bone marrow. PU.1 controls hematopoietic differentiation through physical interactions with other ... ...

    Abstract The Ets transcription factor PU.1 is essential for inducing the differentiation of monocytes, macrophages, and B cells in fetal liver and adult bone marrow. PU.1 controls hematopoietic differentiation through physical interactions with other transcription factors, such as C/EBPα and the AP-1 family member c-Jun. We found that PU.1 recruits c-Jun to promoters without the AP-1 binding sites. To address the functional importance of this interaction, we generated PU.1 point mutants that do not bind c-Jun while maintaining normal DNA binding affinity. These mutants lost the ability to transactivate a target reporter that requires a physical PU.1-c-Jun interaction, and did not induce monocyte/macrophage differentiation of PU.1-deficient cells. Knock-in mice carrying these point mutations displayed an almost complete block in hematopoiesis and perinatal lethality. While the PU.1 mutants were expressed in hematopoietic stem and early progenitor cells, myeloid differentiation was severely blocked, leading to an almost complete loss of mature hematopoietic cells. Differentiation into mature macrophages could be restored by expressing PU.1 mutant fused to c-Jun, demonstrating that a physical PU.1-c-Jun interaction is crucial for the transactivation of PU.1 target genes required for myeloid commitment and normal PU.1 function in vivo during macrophage differentiation.
    MeSH term(s) Animals ; Binding Sites ; Cell Differentiation/genetics ; Hematopoiesis/genetics ; Mice ; Promoter Regions, Genetic ; Proto-Oncogene Proteins c-jun ; Transcription Factor AP-1/genetics
    Chemical Substances Proto-Oncogene Proteins c-jun ; Transcription Factor AP-1
    Language English
    Publishing date 2022-09-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-03888-7
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  3. Article ; Online: NAD Modulates DNA Methylation and Cell Differentiation.

    Ummarino, Simone / Hausman, Clinton / Gaggi, Giulia / Rinaldi, Lucrezia / Bassal, Mahmoud A / Zhang, Yanzhou / Seelam, Andy Joe / Kobayashi, Ikei S / Borchiellini, Marta / Ebralidze, Alexander K / Ghinassi, Barbara / Trinh, Bon Q / Kobayashi, Susumu S / Di Ruscio, Annalisa

    Cells

    2021  Volume 10, Issue 11

    Abstract: Nutritional intake impacts the human epigenome by directing epigenetic pathways in normal cell development via as yet unknown molecular mechanisms. Consequently, imbalance in the nutritional intake is able to dysregulate the epigenetic profile and drive ... ...

    Abstract Nutritional intake impacts the human epigenome by directing epigenetic pathways in normal cell development via as yet unknown molecular mechanisms. Consequently, imbalance in the nutritional intake is able to dysregulate the epigenetic profile and drive cells towards malignant transformation. Here we present a novel epigenetic effect of the essential nutrient, NAD. We demonstrate that impairment of DNMT1 enzymatic activity by NAD-promoted ADP-ribosylation leads to demethylation and transcriptional activation of the
    MeSH term(s) CCAAT-Enhancer-Binding Proteins/genetics ; CCAAT-Enhancer-Binding Proteins/metabolism ; Cell Differentiation/drug effects ; Cell Line ; DNA Demethylation/drug effects ; DNA Methylation/genetics ; Humans ; Mitochondria/drug effects ; Mitochondria/metabolism ; Myeloid Cells/cytology ; Myeloid Cells/drug effects ; NAD/pharmacology ; Neoplasms/genetics ; Neoplasms/pathology ; Oxidative Phosphorylation/drug effects ; Poly Adenosine Diphosphate Ribose/metabolism ; Poly(ADP-ribose) Polymerases/metabolism ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transcription, Genetic/drug effects
    Chemical Substances CCAAT-Enhancer-Binding Proteins ; CEBPA protein, human ; RNA, Messenger ; NAD (0U46U6E8UK) ; Poly Adenosine Diphosphate Ribose (26656-46-2) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
    Language English
    Publishing date 2021-11-02
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10112986
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  4. Article ; Online: The homeobox gene DLX4 regulates erythro-megakaryocytic differentiation by stimulating IL-1β and NF-κB signaling.

    Trinh, Bon Q / Barengo, Nicolas / Kim, Sang Bae / Lee, Ju-Seog / Zweidler-McKay, Patrick A / Naora, Honami

    Journal of cell science

    2015  Volume 128, Issue 16, Page(s) 3055–3067

    Abstract: Megakaryocyte and erythroid development are tightly controlled by a repertoire of cytokines, but it is not clear how cytokine-activated signaling pathways are controlled during development of these two lineages. Here, we identify that expression of DLX4, ...

    Abstract Megakaryocyte and erythroid development are tightly controlled by a repertoire of cytokines, but it is not clear how cytokine-activated signaling pathways are controlled during development of these two lineages. Here, we identify that expression of DLX4, a transcription factor encoded by a homeobox gene, increases during megakaryopoiesis but decreases during erythropoiesis. Enforced expression of DLX4 in CD34(+) stem and progenitor cells and in bipotent K562 cells induced lineage markers and morphologic features of megakaryocytes and repressed erythroid marker expression and hemoglobin levels. Converse results were obtained when DLX4 was knocked down. Gene Ontology and Gene Set Enrichment Analyses of genome-wide changes in gene expression revealed that DLX4 induces a megakaryocytic transcriptional program and inhibits an erythroid transcriptional program. DLX4 also induced gene signatures that are associated with nuclear factor κB (NF-κB) signaling. The ability of DLX4 to promote megakaryocyte development at the expense of erythroid generation was diminished by blocking NF-κB activity or by repressing IL1B, a transcriptional target of DLX4. Collectively, our findings indicate that DLX4 exerts opposing effects on the megakaryocytic and erythroid lineages in part by inducing IL-1β and NF-κB signaling.
    MeSH term(s) Cell Differentiation/genetics ; Cell Lineage/genetics ; Erythrocytes/cytology ; Erythrocytes/metabolism ; Erythropoiesis/genetics ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/biosynthesis ; Homeodomain Proteins/genetics ; Humans ; Interleukin-1beta/antagonists & inhibitors ; Interleukin-1beta/genetics ; K562 Cells ; Megakaryocyte-Erythroid Progenitor Cells/cytology ; Megakaryocytes/cytology ; Megakaryocytes/metabolism ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/genetics ; Signal Transduction ; Stem Cells/cytology ; Stem Cells/metabolism ; Transcription Factors/biosynthesis ; Transcription Factors/genetics
    Chemical Substances DLX4 protein, human ; Homeodomain Proteins ; IL1B protein, human ; Interleukin-1beta ; NF-kappa B ; Transcription Factors
    Language English
    Publishing date 2015-07-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.168187
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  5. Article ; Online: Dual functions of the homeoprotein DLX4 in modulating responsiveness of tumor cells to topoisomerase II-targeting drugs.

    Trinh, Bon Q / Ko, Song Yi / Barengo, Nicolas / Lin, Shiaw-Yih / Naora, Honami

    Cancer research

    2012  Volume 73, Issue 2, Page(s) 1000–1010

    Abstract: Topoisomerase II (TOP2)-targeting poisons such as anthracyclines and etoposide are commonly used for cancer chemotherapy and kill tumor cells by causing accumulation of DNA double-strand breaks (DSB). Several lines of evidence indicate that ... ...

    Abstract Topoisomerase II (TOP2)-targeting poisons such as anthracyclines and etoposide are commonly used for cancer chemotherapy and kill tumor cells by causing accumulation of DNA double-strand breaks (DSB). Several lines of evidence indicate that overexpression of TOP2A, the gene encoding topoisomerase IIα, increases sensitivity of tumor cells to TOP2 poisons, but it is not clear why some TOP2A-overexpressing (TOP2A-High) tumors respond poorly to these drugs. In this study, we identified that TOP2A expression is induced by DLX4, a homeoprotein that is overexpressed in breast and ovarian cancers. Analysis of breast cancer datasets revealed that TOP2A-high cases that also highly expressed DLX4 responded more poorly to anthracycline-based chemotherapy than TOP2A-high cases that expressed DLX4 at low levels. Overexpression of TOP2A alone in tumor cells increased the level of DSBs induced by TOP2 poisons. In contrast, DLX4 reduced the level of TOP2 poison-induced DSBs irrespective of its induction of TOP2A. DLX4 did not stimulate homologous recombination-mediated repair of DSBs. However, DLX4 interacted with Ku proteins, stimulated DNA-dependent protein kinase activity, and increased erroneous end-joining repair of DSBs. Whereas DLX4 did not reduce levels of TOP2 poison-induced DSBs in Ku-deficient cells, DLX4 stimulated DSB repair and reduced the level of TOP2 poison-induced DSBs when Ku was reconstituted in these cells. Our findings indicate that DLX4 induces TOP2A expression but reduces sensitivity of tumor cells to TOP2 poisons by stimulating Ku-dependent repair of DSBs. These opposing activities of DLX4 could explain why some TOP2A-overexpressing tumors are not highly sensitive to TOP2 poisons.
    MeSH term(s) Anthracyclines/pharmacology ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Breast Neoplasms/genetics ; Cell Line, Tumor ; DNA Breaks, Double-Stranded ; DNA Helicases/metabolism ; DNA Repair ; DNA Topoisomerases, Type II/drug effects ; DNA Topoisomerases, Type II/genetics ; DNA Topoisomerases, Type II/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Drug Resistance, Neoplasm ; Homeodomain Proteins/genetics ; Humans ; Ku Autoantigen ; Poly-ADP-Ribose Binding Proteins ; Transcription Factors/genetics
    Chemical Substances Anthracyclines ; Antigens, Neoplasm ; DLX4 protein, human ; DNA-Binding Proteins ; Homeodomain Proteins ; Poly-ADP-Ribose Binding Proteins ; Transcription Factors ; DNA Helicases (EC 3.6.4.-) ; XRCC5 protein, human (EC 3.6.4.12) ; Ku Autoantigen (EC 4.2.99.-) ; DNA Topoisomerases, Type II (EC 5.99.1.3) ; TOP2A protein, human (EC 5.99.1.3)
    Language English
    Publishing date 2012-12-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-12-3538
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  6. Article ; Online: Myeloid lncRNA LOUP mediates opposing regulatory effects of RUNX1 and RUNX1-ETO in t(8;21) AML.

    Trinh, Bon Q / Ummarino, Simone / Zhang, Yanzhou / Ebralidze, Alexander K / Bassal, Mahmoud A / Nguyen, Tuan M / Heller, Gerwin / Coffey, Rory / Tenen, Danielle E / van der Kouwe, Emiel / Fabiani, Emiliano / Gurnari, Carmelo / Wu, Chan-Shuo / Angarica, Vladimir Espinosa / Yang, Henry / Chen, Sisi / Zhang, Hong / Thurm, Abby R / Marchi, Francisco /
    Levantini, Elena / Staber, Philipp B / Zhang, Pu / Voso, Maria Teresa / Pandolfi, Pier Paolo / Kobayashi, Susumu S / Chai, Li / Di Ruscio, Annalisa / Tenen, Daniel G

    Blood

    2021  Volume 138, Issue 15, Page(s) 1331–1344

    Abstract: The mechanism underlying cell type-specific gene induction conferred by ubiquitous transcription factors as well as disruptions caused by their chimeric derivatives in leukemia is not well understood. Here, we investigate whether RNAs coordinate with ... ...

    Abstract The mechanism underlying cell type-specific gene induction conferred by ubiquitous transcription factors as well as disruptions caused by their chimeric derivatives in leukemia is not well understood. Here, we investigate whether RNAs coordinate with transcription factors to drive myeloid gene transcription. In an integrated genome-wide approach surveying for gene loci exhibiting concurrent RNA and DNA interactions with the broadly expressed Runt-related transcription factor 1 (RUNX1), we identified the long noncoding RNA (lncRNA) originating from the upstream regulatory element of PU.1 (LOUP). This myeloid-specific and polyadenylated lncRNA induces myeloid differentiation and inhibits cell growth, acting as a transcriptional inducer of the myeloid master regulator PU.1. Mechanistically, LOUP recruits RUNX1 to both the PU.1 enhancer and the promoter, leading to the formation of an active chromatin loop. In t(8;21) acute myeloid leukemia (AML), wherein RUNX1 is fused to ETO, the resulting oncogenic fusion protein, RUNX1-ETO, limits chromatin accessibility at the LOUP locus, causing inhibition of LOUP and PU.1 expression. These findings highlight the important role of the interplay between cell-type-specific RNAs and transcription factors, as well as their oncogenic derivatives in modulating lineage-gene activation and raise the possibility that RNA regulators of transcription factors represent alternative targets for therapeutic development.
    MeSH term(s) Cell Line, Tumor ; Core Binding Factor Alpha 2 Subunit/genetics ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Oncogene Proteins, Fusion/genetics ; RNA, Long Noncoding/genetics ; RUNX1 Translocation Partner 1 Protein/genetics ; Transcriptional Activation
    Chemical Substances Core Binding Factor Alpha 2 Subunit ; Oncogene Proteins, Fusion ; RNA, Long Noncoding ; RUNX1 Translocation Partner 1 Protein ; RUNX1 protein, human ; RUNX1T1 protein, human
    Language English
    Publishing date 2021-05-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020007920
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  7. Article ; Online: A novel hTERT promoter-driven E1A therapeutic for ovarian cancer.

    Xie, Xiaoming / Hsu, Jennifer L / Choi, Min-Gew / Xia, Weiya / Yamaguchi, Hirohito / Chen, Chun-Te / Trinh, Bon Q / Lu, Zhen / Ueno, Naoto T / Wolf, Judith K / Bast, Robert C / Hung, Mien-Chie

    Molecular cancer therapeutics

    2009  Volume 8, Issue 8, Page(s) 2375–2382

    Abstract: Currently, an effective gene therapy strategy, which not only retains cancer-specific expression but also limits toxicity, has yet to be developed for ovarian cancer. Mounting reports over the years have shown that human telomerase activity is ... ...

    Abstract Currently, an effective gene therapy strategy, which not only retains cancer-specific expression but also limits toxicity, has yet to be developed for ovarian cancer. Mounting reports over the years have shown that human telomerase activity is significantly elevated in cancer cells compared with normal cells. In this study, we evaluated the human telomerase reverse transcriptase (hTERT; T) promoter and showed that it can direct target gene expression preferentially in ovarian cancer cells. However, its promoter (T) activity is much lower than that of cytomegalovirus (CMV), a commonly used nonspecific promoter. To overcome this problem, we have integrated the T promoter into our recently developed VP16-Gal4-WPRE integrated systemic amplifier (VISA) system and dramatically enhanced transgene expression. In addition, to further develop this cancer-specific promoter gene expression system into an applicable therapeutic vector, we expressed E1A (an adenoviral type 5 transcription factor that possesses anticancer properties) through this novel VISA platform. We showed that the T-VISA system specifically targeted the expression of E1A to ovarian cancer cells at a level greater than or comparable with the commonly used CMV promoter, yet remained nearly silent in normal cells, thus making this a suitable gene therapy construct. By using this cancer-specific promoter that limits target gene expression in normal cells/tissues, potential toxicity induced by the CMV promoter would be prevented. More importantly, we showed significant antitumor activity with much less toxicity in animal models through i.v. delivery of T-VISA-E1A:liposomal nanoparticles, suggesting a promising role of T-VISA-E1A for ovarian cancer treatment under a gene therapy setting.
    MeSH term(s) Adenovirus E1A Proteins/genetics ; Animals ; Cell Line, Tumor ; Female ; Genetic Therapy/methods ; Genetic Vectors/genetics ; Genetic Vectors/metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Ovarian Neoplasms/therapy ; Promoter Regions, Genetic ; Telomerase/genetics ; Telomerase/metabolism ; Transfection
    Chemical Substances Adenovirus E1A Proteins ; TERT protein, human (EC 2.7.7.49) ; Telomerase (EC 2.7.7.49)
    Language English
    Publishing date 2009-08-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-09-0056
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