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  1. Article ; Online: Author Correction: Systematic profiling of conditional pathway activation identifies context-dependent synthetic lethalities.

    Chang, Liang / Jung, Nancy Y / Atari, Adel / Rodriguez, Diego J / Kesar, Devishi / Song, Tian-Yu / Rees, Matthew G / Ronan, Melissa / Li, Ruitong / Ruiz, Paloma / Chaturantabut, Saireudee / Ito, Takahiro / van Tienen, Laurens M / Tseng, Yuen-Yi / Roth, Jennifer A / Sellers, William R

    Nature genetics

    2024  Volume 56, Issue 3, Page(s) 553

    Language English
    Publishing date 2024-02-24
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-024-01680-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Systematic profiling of conditional pathway activation identifies context-dependent synthetic lethalities.

    Chang, Liang / Jung, Nancy Y / Atari, Adel / Rodriguez, Diego J / Kesar, Devishi / Song, Tian-Yu / Rees, Matthew G / Ronan, Melissa / Li, Ruitong / Ruiz, Paloma / Chaturantabut, Saireudee / Ito, Takahiro / van Tienen, Laurens M / Tseng, Yuen-Yi / Roth, Jennifer A / Sellers, William R

    Nature genetics

    2023  Volume 55, Issue 10, Page(s) 1709–1720

    Abstract: The paradigm of cancer-targeted therapies has focused largely on inhibition of critical pathways in cancer. Conversely, conditional activation of signaling pathways as a new source of selective cancer vulnerabilities has not been deeply characterized. In ...

    Abstract The paradigm of cancer-targeted therapies has focused largely on inhibition of critical pathways in cancer. Conversely, conditional activation of signaling pathways as a new source of selective cancer vulnerabilities has not been deeply characterized. In this study, we sought to systematically identify context-specific gene-activation-induced lethalities in cancer. To this end, we developed a method for gain-of-function genetic perturbations simultaneously across ~500 barcoded cancer cell lines. Using this approach, we queried the pan-cancer vulnerability landscape upon activating ten key pathway nodes, revealing selective activation dependencies of MAPK and PI3K pathways associated with specific biomarkers. Notably, we discovered new pathway hyperactivation dependencies in subsets of APC-mutant colorectal cancers where further activation of the WNT pathway by APC knockdown or direct β-catenin overexpression led to robust antitumor effects in xenograft and patient-derived organoid models. Together, this study reveals a new class of conditional gene-activation dependencies in cancer.
    MeSH term(s) Humans ; Colorectal Neoplasms/pathology ; Phosphatidylinositol 3-Kinases ; beta Catenin/genetics ; Wnt Signaling Pathway/genetics ; Cell Proliferation ; Cell Line, Tumor
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; beta Catenin
    Language English
    Publishing date 2023-09-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-023-01515-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Estrogen Acts Through Estrogen Receptor 2b to Regulate Hepatobiliary Fate During Vertebrate Development.

    Chaturantabut, Saireudee / Shwartz, Arkadi / Garnaas, Maija K / LaBella, Kyle / Li, Chia-Cheng / Carroll, Kelli J / Cutting, Claire C / Budrow, Nadine / Palaria, Amrita / Gorelick, Daniel A / Tremblay, Kimberly D / North, Trista E / Goessling, Wolfram

    Hepatology (Baltimore, Md.)

    2020  Volume 72, Issue 5, Page(s) 1786–1799

    Abstract: Background and aims: During liver development, bipotent progenitor cells differentiate into hepatocytes and biliary epithelial cells to ensure a functional liver required to maintain organismal homeostasis. The developmental cues controlling the ... ...

    Abstract Background and aims: During liver development, bipotent progenitor cells differentiate into hepatocytes and biliary epithelial cells to ensure a functional liver required to maintain organismal homeostasis. The developmental cues controlling the differentiation of committed progenitors into these cell types, however, are incompletely understood. Here, we discover an essential role for estrogenic regulation in vertebrate liver development to affect hepatobiliary fate decisions.
    Approach and results: Exposure of zebrafish embryos to 17β-estradiol (E2) during liver development significantly decreased hepatocyte-specific gene expression, liver size, and hepatocyte number. In contrast, pharmacological blockade of estrogen synthesis or nuclear estrogen receptor (ESR) signaling enhanced liver size and hepatocyte marker expression. Transgenic reporter fish demonstrated nuclear ESR activity in the developing liver. Chemical inhibition and morpholino knockdown of nuclear estrogen receptor 2b (esr2b) increased hepatocyte gene expression and blocked the effects of E2 exposure. esr2b
    Conclusions: Our studies identify E2, esr2b, and downstream BMP activity as important regulators of hepatobiliary fate decisions during vertebrate liver development. These results have significant clinical implications for liver development in infants exposed to abnormal estrogen levels or estrogenic compounds during pregnancy.
    MeSH term(s) Animals ; Animals, Genetically Modified ; Biliary Tract/cytology ; Biliary Tract/embryology ; Biliary Tract/metabolism ; Cell Differentiation/genetics ; Cell Line ; Embryo, Nonmammalian ; Estradiol/administration & dosage ; Estradiol/metabolism ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Female ; Gene Expression Regulation, Developmental ; Gene Knockdown Techniques ; Hepatocytes/physiology ; Liver/cytology ; Liver/embryology ; Liver/metabolism ; Male ; Models, Animal ; Morpholinos/administration & dosage ; Morpholinos/genetics ; Signal Transduction/genetics ; Stem Cells/physiology ; Zebrafish ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances Estrogen Receptor beta ; Morpholinos ; Zebrafish Proteins ; estrogen receptor 2b, zebrafish ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2020-02-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31184
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Estrogen Activation of G-Protein-Coupled Estrogen Receptor 1 Regulates Phosphoinositide 3-Kinase and mTOR Signaling to Promote Liver Growth in Zebrafish and Proliferation of Human Hepatocytes.

    Chaturantabut, Saireudee / Shwartz, Arkadi / Evason, Kimberley J / Cox, Andrew G / Labella, Kyle / Schepers, Arnout G / Yang, Song / Acuña, Mariana / Houvras, Yariv / Mancio-Silva, Liliana / Romano, Shannon / Gorelick, Daniel A / Cohen, David E / Zon, Leonard I / Bhatia, Sangeeta N / North, Trista E / Goessling, Wolfram

    Gastroenterology

    2019  Volume 156, Issue 6, Page(s) 1788–1804.e13

    Abstract: Background & aims: Patients with cirrhosis are at high risk for hepatocellular carcinoma (HCC) and often have increased serum levels of estrogen. It is not clear how estrogen promotes hepatic growth. We investigated the effects of estrogen on hepatocyte ...

    Abstract Background & aims: Patients with cirrhosis are at high risk for hepatocellular carcinoma (HCC) and often have increased serum levels of estrogen. It is not clear how estrogen promotes hepatic growth. We investigated the effects of estrogen on hepatocyte proliferation during zebrafish development, liver regeneration, and carcinogenesis. We also studied human hepatocytes and liver tissues.
    Methods: Zebrafish were exposed to selective modifiers of estrogen signaling at larval and adult stages. Liver growth was assessed by gene expression, fluorescent imaging, and histologic analyses. We monitored liver regeneration after hepatocyte ablation and HCC development after administration of chemical carcinogens (dimethylbenzanthrazene). Proliferation of human hepatocytes was measured in a coculture system. We measured levels of G-protein-coupled estrogen receptor (GPER1) in HCC and nontumor liver tissues from 68 patients by immunohistochemistry.
    Results: Exposure to 17β-estradiol (E2) increased proliferation of hepatocytes and liver volume and mass in larval and adult zebrafish. Chemical genetic and epistasis experiments showed that GPER1 mediates the effects of E2 via the phosphoinositide 3-kinase-protein kinase B-mechanistic target of rapamycin pathway: gper1-knockout and mtor-knockout zebrafish did not increase liver growth in response to E2. HCC samples from patients had increased levels of GPER1 compared with nontumor tissue samples; estrogen promoted proliferation of human primary hepatocytes. Estrogen accelerated hepatocarcinogenesis specifically in male zebrafish. Chemical inhibition or genetic loss of GPER1 significantly reduced tumor development in the zebrafish.
    Conclusions: In an analysis of zebrafish and human liver cells and tissues, we found GPER1 to be a hepatic estrogen sensor that regulates liver growth during development, regeneration, and tumorigenesis. Inhibitors of GPER1 might be developed for liver cancer prevention or treatment.
    Transcript profiling: The accession number in the Gene Expression Omnibus is GSE92544.
    MeSH term(s) 9,10-Dimethyl-1,2-benzanthracene ; Animals ; Carcinogenesis/drug effects ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Proliferation/drug effects ; Estradiol/pharmacology ; Estrogens/pharmacology ; Female ; Gene Expression/drug effects ; Hepatocytes ; Humans ; Liver/growth & development ; Liver/metabolism ; Liver Cirrhosis/metabolism ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Liver Regeneration ; Male ; Organ Size/drug effects ; Phosphatidylinositol 3-Kinase/metabolism ; Receptors, Estrogen/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Sex Factors ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Tumor Burden/drug effects ; Zebrafish ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
    Chemical Substances Estrogens ; GPER1 protein, human ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Zebrafish Proteins ; gper1 protein, zebrafish ; Estradiol (4TI98Z838E) ; 9,10-Dimethyl-1,2-benzanthracene (57-97-6) ; MTOR protein, human (EC 2.7.1.1) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; mTOR protein, zebrafish (EC 2.7.11.1)
    Language English
    Publishing date 2019-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2019.01.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Synthesis and characterization of water-soluble free-base, zinc and copper porphyrin-oligonucleotide conjugates.

    Mammana, Angela / Asakawa, Tomohiro / Bitsch-Jensen, Klaus / Wolfe, Amanda / Chaturantabut, Saireudee / Otani, Yuko / Li, Xiaoxu / Li, Zengmin / Nakanishi, Koji / Balaz, Milan / Ellestad, George A / Berova, Nina

    Bioorganic & medicinal chemistry

    2008  Volume 16, Issue 13, Page(s) 6544–6551

    Abstract: We describe the synthesis and characterization of a series of water-soluble free-base, zinc, and copper porphyrin-oligonucleotide (ODN) conjugates. A non-charged tetraarylporphyrin was directly attached to the 5'-position of thymine via a short amide ... ...

    Abstract We describe the synthesis and characterization of a series of water-soluble free-base, zinc, and copper porphyrin-oligonucleotide (ODN) conjugates. A non-charged tetraarylporphyrin was directly attached to the 5'-position of thymine via a short amide linker. Such a linker should allow for rigid connection to the adjacent nucleobases, thus increasing the sensitivity for monitoring conformational changes of the ODNs by electronic circular dichroism due to capping effects or ligand binding. Two complementary synthetic approaches have been used to incorporate porphyrin chromophores into the DNA. In the first approach a porphyrin carboxylic acid is conjugated to 5'-amino-ODN. In the second approach the phosphoramidite of the porphyrin-amido-thymidine is coupled to 5'-hydroxy-ODN using standard automated phosphoramidite chemistry. In both cases a spontaneous metallation of the free-base porphyrin in porphyrin-DNA conjugates was observed during the porphyrin-DNA conjugate cleavage from the solid support and its consequent deprotection using concentrated aqueous ammonia. Zinc and copper porphyrin-DNA conjugates were isolated by HPLC and characterized together with the anticipated free-base porphyrin-DNA conjugate. Authentic zinc and copper porphyrin-DNA conjugates were intentionally prepared from intentionally metallated porphyrins to compare their spectroscopic and HPLC characteristics with isolated metallospecies and to confirm the spontaneous metallation.
    MeSH term(s) Chromatography, High Pressure Liquid ; Copper/chemistry ; DNA/chemistry ; Magnetic Resonance Spectroscopy ; Metalloporphyrins/chemistry ; Molecular Structure ; Oligonucleotides/chemical synthesis ; Oligonucleotides/chemistry ; Solubility ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Spectrophotometry ; Water/chemistry ; Zinc/chemistry
    Chemical Substances Metalloporphyrins ; Oligonucleotides ; Water (059QF0KO0R) ; Copper (789U1901C5) ; DNA (9007-49-2) ; Zinc (J41CSQ7QDS)
    Language English
    Publishing date 2008-07-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1161284-8
    ISSN 1464-3391 ; 0968-0896
    ISSN (online) 1464-3391
    ISSN 0968-0896
    DOI 10.1016/j.bmc.2008.05.041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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