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  1. Article ; Online: Cell surface GRP78 and Dermcidin cooperate to regulate breast cancer cell migration through Wnt signaling.

    Lager, Tyson W / Conner, Clay / Keating, Claudia R / Warshaw, Jane N / Panopoulos, Athanasia D

    Oncogene

    2021  Volume 40, Issue 23, Page(s) 4050–4059

    Abstract: The heat shock protein GRP78 typically resides in the endoplasmic reticulum in normal tissues, but it has been shown to be expressed on the cell surface of several cancer cells, and some stem cells, where it can act as a signaling molecule by not-yet- ... ...

    Abstract The heat shock protein GRP78 typically resides in the endoplasmic reticulum in normal tissues, but it has been shown to be expressed on the cell surface of several cancer cells, and some stem cells, where it can act as a signaling molecule by not-yet-fully defined mechanisms. Although cell surface GRP78 (sGRP78) has emerged as an attractive chemotherapeutic target, understanding how sGRP78 is functioning in cancer has been complicated by the fact that sGRP78 can function in a cell-context dependent manner, with a diverse array of reported binding partners, to regulate a variety of cellular responses. We had previously shown that sGRP78 was important in regulating pluripotent stem cell (PSC) functions, and hypothesized that embryonic-like mechanisms of GRP78 were critical to regulating aggressive breast cancer cell functions. Here, using proteomics we identify Dermcidin (DCD) as a novel sGRP78 binding partner common to both PSCs and breast cancer cells. We show that GRP78 and DCD cooperate to regulate stem cell and cancer cell migration that is dependent on the cell surface functions of these proteins. Finally, we identify Wnt/β-catenin signaling, a critical pathway in stem cell and cancer cell biology, as an important downstream intermediate in regulating this migration phenotype.
    MeSH term(s) Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Membrane/metabolism ; Cell Movement/physiology ; Cell Proliferation/physiology ; Endoplasmic Reticulum Chaperone BiP/metabolism ; Female ; Humans ; Peptides/metabolism ; Stem Cells/metabolism ; Wnt Signaling Pathway
    Chemical Substances Endoplasmic Reticulum Chaperone BiP ; HSPA5 protein, human ; Peptides ; dermcidin
    Language English
    Publishing date 2021-05-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-021-01821-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: An iPSC line derived from a human acute myeloid leukemia cell line (HL-60-iPSC) retains leukemic abnormalities and displays myeloid differentiation defects.

    Yamasaki, Amanda E / Warshaw, Jane N / Kyalwazi, Beverly L / Matsui, Hiroko / Jepsen, Kristen / Panopoulos, Athanasia D

    Stem cell research

    2020  Volume 49, Page(s) 102096

    Abstract: Cancer-derived iPSCs have provided valuable insight into oncogenesis, but human cancer cells can often be difficult to reprogram, especially in cases of complex genetic abnormalities. Here we report, to our knowledge, the first successful generation of ... ...

    Abstract Cancer-derived iPSCs have provided valuable insight into oncogenesis, but human cancer cells can often be difficult to reprogram, especially in cases of complex genetic abnormalities. Here we report, to our knowledge, the first successful generation of an iPSC line from a human immortalized acute myeloid leukemia (AML) cell line, the cell line HL-60. This iPSC line retains a majority of the leukemic genotype and displays defects in myeloid differentiation, thus providing a tool for modeling and studying AML.
    MeSH term(s) Cell Differentiation ; HL-60 Cells ; Hematopoiesis ; Humans ; Induced Pluripotent Stem Cells ; Leukemia, Myeloid, Acute/genetics
    Language English
    Publishing date 2020-11-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1876-7753
    ISSN (online) 1876-7753
    DOI 10.1016/j.scr.2020.102096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: ATRX promotes heterochromatin formation to protect cells from G-quadruplex DNA-mediated stress.

    Teng, Yu-Ching / Sundaresan, Aishwarya / O'Hara, Ryan / Gant, Vincent U / Li, Minhua / Martire, Sara / Warshaw, Jane N / Basu, Amrita / Banaszynski, Laura A

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 3887

    Abstract: ATRX is a tumor suppressor that has been associated with protection from DNA replication stress, purportedly through resolution of difficult-to-replicate G-quadruplex (G4) DNA structures. While several studies demonstrate that loss of ATRX sensitizes ... ...

    Abstract ATRX is a tumor suppressor that has been associated with protection from DNA replication stress, purportedly through resolution of difficult-to-replicate G-quadruplex (G4) DNA structures. While several studies demonstrate that loss of ATRX sensitizes cells to chemical stabilizers of G4 structures, the molecular function of ATRX at G4 regions during replication remains unknown. Here, we demonstrate that ATRX associates with a number of the MCM replication complex subunits and that loss of ATRX leads to G4 structure accumulation at newly synthesized DNA. We show that both the helicase domain of ATRX and its H3.3 chaperone function are required to protect cells from G4-induced replicative stress. Furthermore, these activities are upstream of heterochromatin formation mediated by the histone methyltransferase, ESET, which is the critical molecular event that protects cells from G4-mediated stress. In support, tumors carrying mutations in either ATRX or ESET show increased mutation burden at G4-enriched DNA sequences. Overall, our study provides new insights into mechanisms by which ATRX promotes genome stability with important implications for understanding impacts of its loss on human disease.
    MeSH term(s) Cells, Cultured ; Chromatin Immunoprecipitation Sequencing/methods ; DNA/chemistry ; DNA/genetics ; DNA/metabolism ; DNA Helicases/genetics ; DNA Helicases/metabolism ; DNA Replication/genetics ; G-Quadruplexes ; Genomic Instability/genetics ; HeLa Cells ; Heterochromatin/genetics ; Histones/genetics ; Histones/metabolism ; Humans ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Mutation ; Nucleic Acid Conformation ; X-linked Nuclear Protein/genetics ; X-linked Nuclear Protein/metabolism
    Chemical Substances Heterochromatin ; Histones ; Molecular Chaperones ; DNA (9007-49-2) ; DNA Helicases (EC 3.6.4.-) ; ATRX protein, human (EC 3.6.4.12) ; X-linked Nuclear Protein (EC 3.6.4.12)
    Language English
    Publishing date 2021-06-23
    Publishing country England
    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 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-24206-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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