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  1. Article ; Online: Integrin-independent support of cancer drug resistance by tetraspanin CD151.

    Hwang, Soonyean / Takimoto, Takayuki / Hemler, Martin E

    Cellular and molecular life sciences : CMLS

    2019  Volume 76, Issue 8, Page(s) 1595–1604

    Abstract: Tetraspanin protein CD151 has typically been studied as binding partner and functional regulator of laminin-binding integrins. However, we show here that CD151 supports anti-cancer drug resistance independent of integrins. CD151 ablation sensitized ... ...

    Abstract Tetraspanin protein CD151 has typically been studied as binding partner and functional regulator of laminin-binding integrins. However, we show here that CD151 supports anti-cancer drug resistance independent of integrins. CD151 ablation sensitized multiple tumor cell types to several anti-cancer drugs (e.g., gefitinib and camptothecin), thus increasing apoptosis, as seen using cleaved caspase-3, cleaved PARP (poly (ADP-ribose) polymerase), annexin V, and propidium iodide staining assays. Drug sensitization due to CD151 ablation is integrin-independent, because, (1) effects occurred in cells when integrins were unengaged with ligand, (2) integrin ablation (α3 and α6 subunits) did not mimic effects of CD151 ablation, (3) the CD151
    MeSH term(s) A549 Cells ; Antineoplastic Agents/administration & dosage ; Apoptosis/drug effects ; Camptothecin/administration & dosage ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Gefitinib/administration & dosage ; Humans ; Integrins/metabolism ; Laminin/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Tetraspanin 24/genetics ; Tetraspanin 24/metabolism
    Chemical Substances Antineoplastic Agents ; CD151 protein, human ; Integrins ; Laminin ; RNA, Messenger ; Tetraspanin 24 ; Gefitinib (S65743JHBS) ; Camptothecin (XT3Z54Z28A)
    Language English
    Publishing date 2019-02-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03014-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Integrin-independent support of cancer drug resistance by tetraspanin CD151

    Hwang, Soonyean / Takimoto, Takayuki / Hemler, Martin E

    Cellular and molecular life sciences. 2019 Apr., v. 76, no. 8

    2019  

    Abstract: Tetraspanin protein CD151 has typically been studied as binding partner and functional regulator of laminin-binding integrins. However, we show here that CD151 supports anti-cancer drug resistance independent of integrins. CD151 ablation sensitized ... ...

    Abstract Tetraspanin protein CD151 has typically been studied as binding partner and functional regulator of laminin-binding integrins. However, we show here that CD151 supports anti-cancer drug resistance independent of integrins. CD151 ablation sensitized multiple tumor cell types to several anti-cancer drugs (e.g., gefitinib and camptothecin), thus increasing apoptosis, as seen using cleaved caspase-3, cleaved PARP (poly (ADP-ribose) polymerase), annexin V, and propidium iodide staining assays. Drug sensitization due to CD151 ablation is integrin-independent, because, (1) effects occurred in cells when integrins were unengaged with ligand, (2) integrin ablation (α3 and α6 subunits) did not mimic effects of CD151 ablation, (3) the CD151QRD mutant, with diminished integrin association, and CD151WT (unmutated CD151) similarly reconstituted drug protection, and (4) treatment with anti-cancer drugs selectively upregulated intracellular nonintegrin-associated CD151 (NIA-CD151), consistent with its role in drug resistance. Together, these results suggest that upregulated CD151 expression may support not only typical integrin-dependent functions, but also integrin-independent survival of circulating (and possibly metastatic) cancer cells during anti-cancer drug therapy.
    Keywords NAD ADP-ribosyltransferase ; antineoplastic agents ; apoptosis ; caspase-3 ; drug resistance ; drug therapy ; gene expression regulation ; integrins ; ligands ; metastasis ; mutants ; neoplasm cells ; neoplasms ; propidium ; staining
    Language English
    Dates of publication 2019-04
    Size p. 1595-1604.
    Publishing place Springer International Publishing
    Document type Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-019-03014-7
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  3. Article ; Online: MicroRNAs as an emerging target for melanoma therapy.

    Ryu, Byungwoo / Hwang, Soonyean / Alani, Rhoda M

    The Journal of investigative dermatology

    2013  Volume 133, Issue 5, Page(s) 1137–1139

    Abstract: Despite the growing focus on microRNAs (miRNAs) as novel diagnostic tools and therapeutic targets in cancer, global characterization of miRNA expression patterns and their specific targets in melanoma has lagged. In this issue, Reuland et al. (2012) ... ...

    Abstract Despite the growing focus on microRNAs (miRNAs) as novel diagnostic tools and therapeutic targets in cancer, global characterization of miRNA expression patterns and their specific targets in melanoma has lagged. In this issue, Reuland et al. (2012) identify miR-26a as being specifically downregulated in human melanoma cells. They further establish Silencer of Death Domains as a novel target for miR-26a, which functionally mediates melanoma cell death. These findings suggest that miR-26a may serve as a promising novel therapy for subsets of melanoma.
    MeSH term(s) Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Apoptosis/physiology ; Down-Regulation/physiology ; Humans ; Melanoma/metabolism ; MicroRNAs/metabolism ; Skin Neoplasms/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; BAG4 protein, human ; MIRN26A microRNA, human ; MicroRNAs
    Language English
    Publishing date 2013-05
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1038/jid.2012.505
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Notch3 signaling-mediated melanoma-endothelial crosstalk regulates melanoma stem-like cell homeostasis and niche morphogenesis.

    Hsu, Mei-Yu / Yang, Moon Hee / Schnegg, Caroline I / Hwang, Soonyean / Ryu, Byungwoo / Alani, Rhoda M

    Laboratory investigation; a journal of technical methods and pathology

    2017  Volume 97, Issue 6, Page(s) 725–736

    Abstract: Melanoma is among the most virulent cancers, owing to its propensity to metastasize and its resistance to current therapies. The treatment failure is largely attributed to tumor heterogeneity, particularly subpopulations possessing stem cell-like ... ...

    Abstract Melanoma is among the most virulent cancers, owing to its propensity to metastasize and its resistance to current therapies. The treatment failure is largely attributed to tumor heterogeneity, particularly subpopulations possessing stem cell-like properties, ie, melanoma stem-like cells (MSLCs). Evidence indicates that the MSLC phenotype is malleable and may be acquired by non-MSLCs through phenotypic switching upon appropriate stimuli, the so-called 'dynamic stemness'. Since the phenotypic characteristics and functional integrity of MSLCs depend on their vascular niche, using a two-dimensional (2D) melanoma-endothelium co-culture model, where the MSLC niche is recapitulated in vitro, we identified Notch3 signaling pathway as a micro-environmental cue governing MSLC phenotypic plasticity via pathway-specific gene expression arrays. Accordingly, lentiviral shRNA-mediated Notch3 knockdown (KD) in melanoma cell lines exhibiting high levels of endogenous Notch3 led to retarded/abolished tumorigenicity in vivo through both depleting MSLC fractions, evinced by MSLC marker downregulation (eg, CD133 and CD271); and impeding the MSLC niche, corroborated by the attenuated tumor angiogenesis as well as vasculogenic mimicry. In contrast, Notch3 KD affected neither tumor growth nor MSLC subsets in a melanoma cell line with relatively low endogenous Notch3 expression. Thus, Notch3 signaling may facilitate MSLC plasticity and niche morphogenesis in a cell context-dependent manner. Our findings illustrate Notch3 as a molecular switch driving melanoma heterogeneity, and provide the biological rationale for Notch inhibition as a promising therapeutic option.
    MeSH term(s) Animals ; Cell Line, Tumor ; Coculture Techniques ; Human Umbilical Vein Endothelial Cells ; Humans ; Melanoma/metabolism ; Mice ; Neoplastic Stem Cells/metabolism ; Receptor, Notch3/metabolism ; Signal Transduction ; Stem Cell Niche/physiology ; Tumor Microenvironment/physiology
    Chemical Substances Receptor, Notch3
    Language English
    Publishing date 2017-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80178-1
    ISSN 1530-0307 ; 0023-6837
    ISSN (online) 1530-0307
    ISSN 0023-6837
    DOI 10.1038/labinvest.2017.1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Epigenetic Silencing of SPINT2 Promotes Cancer Cell Motility via HGF-MET Pathway Activation in Melanoma.

    Hwang, Soonyean / Kim, Hye-Eun / Min, Michelle / Raghunathan, Rekha / Panova, Izabela P / Munshi, Ruchi / Ryu, Byungwoo

    The Journal of investigative dermatology

    2015  Volume 135, Issue 9, Page(s) 2283–2291

    Abstract: Aberrant HGF-MET (hepatocyte growth factor-met proto-oncogene) signaling activation via interactions with surrounding stromal cells in tumor microenvironment has significant roles in malignant tumor progression. However, extracellular proteolytic ... ...

    Abstract Aberrant HGF-MET (hepatocyte growth factor-met proto-oncogene) signaling activation via interactions with surrounding stromal cells in tumor microenvironment has significant roles in malignant tumor progression. However, extracellular proteolytic regulation of HGF activation, which is influenced by the tumor microenvironment, and its consequential effects on melanoma malignancy remain uncharacterized. In this study, we identified SPINT2 (serine peptidase inhibitor Kunitz type 2), a proteolytic inhibitor of hepatocyte growth factor activator (HGFA), which has a significant role in the suppression of the HGF-MET pathway and malignant melanoma progression. SPINT2 expression is significantly lower in metastatic melanoma tissues compared with those in early-stage primary melanomas, which also corresponded with DNA methylation levels isolated from tissue samples. Treatment with the DNA-hypomethylating agent decitabine in cultured melanoma cells induced transcriptional reactivation of SPINT2, suggesting that this gene is epigenetically silenced in malignant melanomas. Furthermore, we show that ectopically expressed SPINT2 in melanoma cells inhibits the HGF-induced MET-AKT (v-Akt murine thymoma viral oncogene) signaling pathway and decreases malignant phenotype potential such as cell motility and invasive growth of melanoma cells. These results suggest that SPINT2 is associated with tumor-suppressive functions in melanoma by inhibiting an extracellular signal regulator of HGF, which is typically activated by tumor-stromal interactions. These findings indicate that epigenetic impairment of the tightly regulated cytokine-receptor communications in tumor microenvironment may contribute to malignant tumor progression.
    MeSH term(s) Animals ; Cell Movement/genetics ; Cell Proliferation/genetics ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Hepatocyte Growth Factor/genetics ; Hepatocyte Growth Factor/metabolism ; Humans ; Immunoblotting ; Melanoma/genetics ; Melanoma/pathology ; Membrane Glycoproteins/genetics ; Mice ; Mice, Transgenic ; Polymerase Chain Reaction/methods ; Promoter Regions, Genetic ; Serine Endopeptidases ; Signal Transduction/genetics ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Tumor Cells, Cultured
    Chemical Substances Membrane Glycoproteins ; SPINT2 protein, human ; Hepatocyte Growth Factor (67256-21-7) ; HGF activator (EC 3.4.21.-) ; Serine Endopeptidases (EC 3.4.21.-)
    Language English
    Publishing date 2015-09
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1038/jid.2015.160
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  6. Article ; Online: E-cadherin is critical for collective sheet migration and is regulated by the chemokine CXCL12 protein during restitution.

    Hwang, Soonyean / Zimmerman, Noah P / Agle, Kimberle A / Turner, Jerrold R / Kumar, Suresh N / Dwinell, Michael B

    The Journal of biological chemistry

    2012  Volume 287, Issue 26, Page(s) 22227–22240

    Abstract: Chemokines and other immune mediators enhance epithelial barrier repair. The intestinal barrier is established by highly regulated cell-cell contacts between epithelial cells. The goal of these studies was to define the role for the chemokine CXCL12 in ... ...

    Abstract Chemokines and other immune mediators enhance epithelial barrier repair. The intestinal barrier is established by highly regulated cell-cell contacts between epithelial cells. The goal of these studies was to define the role for the chemokine CXCL12 in regulating E-cadherin during collective sheet migration during epithelial restitution. Mechanisms regulating E-cadherin were investigated using Caco2(BBE) and IEC-6 model epithelia. Genetic knockdown confirmed a critical role for E-cadherin in in vitro restitution and in vivo wound repair. During restitution, both CXCL12 and TGF-β1 tightened the monolayer by decreasing the paracellular space between migrating epithelial cells. However, CXCL12 differed from TGF-β1 by stimulating the significant increase in E-cadherin membrane localization during restitution. Chemokine-stimulated relocalization of E-cadherin was paralleled by an increase in barrier integrity of polarized epithelium during restitution. CXCL12 activation of its cognate receptor CXCR4 stimulated E-cadherin localization and monolayer tightening through Rho-associated protein kinase activation and F-actin reorganization. These data demonstrate a key role for E-cadherin in intestinal epithelial restitution.
    MeSH term(s) Actins/metabolism ; Adherens Junctions/metabolism ; Animals ; Caco-2 Cells ; Cadherins/metabolism ; Cell Movement ; Chemokine CXCL12/metabolism ; Chemokines/metabolism ; Epithelium/metabolism ; Gene Deletion ; Heterozygote ; Humans ; Intestinal Mucosa/metabolism ; Microscopy, Confocal/methods ; Rats ; Recombinant Proteins/metabolism ; Wound Healing
    Chemical Substances Actins ; Cadherins ; Chemokine CXCL12 ; Chemokines ; Recombinant Proteins
    Language English
    Publishing date 2012-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M112.367979
    Database MEDical Literature Analysis and Retrieval System OnLINE

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