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  1. Article: Correction: Soung et al. Therapeutic Potential of Chemically Modified MiR-489 in Triple-Negative Breast Cancers.

    Soung, Young Hwa / Chung, Heesung / Yan, Cecilia / Fesler, Andrew / Kim, Hyungjin / Oh, Eok-Soo / Ju, Jingfang / Chung, Jun

    Cancers

    2024  Volume 16, Issue 5

    Abstract: In the original publication [ ... ]. ...

    Abstract In the original publication [...].
    Language English
    Publishing date 2024-02-29
    Publishing country Switzerland
    Document type Published Erratum
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16051010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: The Role of Arrestin Domain-Containing 3 in Regulating Endocytic Recycling and Extracellular Vesicle Sorting of Integrin β4 in Breast Cancer.

    Soung, Young Hwa / Ford, Shane / Yan, Cecilia / Chung, Jun

    Cancers

    2018  Volume 10, Issue 12

    Abstract: Despite the established role of integrin β4 (ITG β4) in breast cancer progression, the importance of endocytic recycling of ITG β4 and its regulatory mechanism are poorly understood. Here, we found that a sub-population of ITG β4 is sorted into early ... ...

    Abstract Despite the established role of integrin β4 (ITG β4) in breast cancer progression, the importance of endocytic recycling of ITG β4 and its regulatory mechanism are poorly understood. Here, we found that a sub-population of ITG β4 is sorted into early endosomes, recycled back to the plasma membrane, and secreted in the form of extracellular vesicles (EVs) upon EGF treatment in triple negative breast cancer (TNBC) cells. A metastasis suppressor, ARRDC3 (arrestin
    Language English
    Publishing date 2018-12-11
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers10120507
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Arrestin Domain Containing 3 Reverses Epithelial to Mesenchymal Transition and Chemo-Resistance of TNBC Cells by Up-Regulating Expression of miR-200b.

    Soung, Young Hwa / Chung, Heesung / Yan, Cecilia / Ju, Jingfang / Chung, Jun

    Cells

    2019  Volume 8, Issue 7

    Abstract: Our previous studies demonstrated the importance of arrestin domain containing 3 (ARRDC3), a metastasis suppressor, in inhibiting invasive and metastatic potential of triple negative breast cancer (TNBC) in vitro and in vivo. However, little is known ... ...

    Abstract Our previous studies demonstrated the importance of arrestin domain containing 3 (ARRDC3), a metastasis suppressor, in inhibiting invasive and metastatic potential of triple negative breast cancer (TNBC) in vitro and in vivo. However, little is known about ARRDC3 mediated transcriptional control and its target genes that are implicated in its metastatic suppressing activity. In this study, we used miRNA array and subsequent functional analyses to identify miRNAs whose expression are significantly regulated by ARRDC3 in TNBC cells. We identified miR-200b as a major target gene of ARRDC3. miR-200b played an essential role in mediating ARRDC3 dependent reversal of EMT phenotypes and chemo-resistance to DNA damaging agents in TNBC cells. Expression of miR-200b also increased the expression of ARRDC3 as well in TNBC cells, suggesting a positive feedback loop between these two molecules. In addition, we combined the therapeutic powers of miR-200b and 5-fluorourancil (5-FU) into a single compound (5-FU-miR-200b) to maximize the synergistic effects of these compounds. Chemically modified miR-200b (5-FU-miR-200b mimic) was more effective in inhibiting metastatic potentials of TNBC cells than unmodified miR-200b and does not require transfection reagents, implying its therapeutic potential in TNBC. Our studies showed the importance of therapeutic targeting ARRDC3/miR-200b pathway in TNBC.
    MeSH term(s) Arrestin/genetics ; Arrestin/metabolism ; Arrestins/genetics ; Arrestins/metabolism ; Cell Line, Tumor ; Cell Movement/physiology ; Drug Resistance, Neoplasm ; Epithelial-Mesenchymal Transition/genetics ; Humans ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Signal Transduction ; Transcriptional Activation ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Up-Regulation
    Chemical Substances ARRDC3 protein, human ; Arrestin ; Arrestins ; MIRN200 microRNA, human ; MicroRNAs
    Language English
    Publishing date 2019-07-10
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells8070692
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Therapeutic Potential of Chemically Modified miR-489 in Triple-Negative Breast Cancers.

    Soung, Young Hwa / Chung, Heesung / Yan, Cecilia / Fesler, Andrew / Kim, Hyungjin / Oh, Eok-Soo / Ju, Jingfang / Chung, Jun

    Cancers

    2020  Volume 12, Issue 8

    Abstract: Triple-negative breast cancers (TNBCs) lack ER, PR and her2 receptors that are targets of common breast cancer therapies with poor prognosis due to their high rates of metastasis and chemoresistance. Based on our previous studies that epigenetic ... ...

    Abstract Triple-negative breast cancers (TNBCs) lack ER, PR and her2 receptors that are targets of common breast cancer therapies with poor prognosis due to their high rates of metastasis and chemoresistance. Based on our previous studies that epigenetic silencing of a potential metastasis suppressor, arrestin domain-containing 3 (ARRDC3), is linked to the aggressive nature of TNBCs, we identified a sub-group of tumor suppressing miRNAs whose expressions were significantly up-regulated by ARRDC3 over-expression in TNBC cells. Among these tumor suppressing miRs, we found that miR-489 is most anti-proliferative in TNBC cells. miR-489 also blocked DNA damaging responses (DDRs) in TNBC cells. To define the mechanism by which miR-489 inhibits TNBC cell functions, we screened the potential target genes of miR-489 and identified MDC-1 and SUZ-12 as novel target genes of miR-489 in TNBC cells. To further exploit the therapeutic potentials of miR-489 in TNBC models, we chemically modified the guide strand of miR-489 (CMM489) by replacing Uracil with 5-fluorouracil (5-FU) so that tumor suppressor (miR-489) and DNA damaging (5-FU) components are combined into a single agent as a novel drug candidate for TNBCs. Our studies demonstrated that CMM489 shows superior effects over miR-489 or 5-FU in inhibition of TNBC cell proliferation and tumor progression, suggesting its therapeutic efficacy in TNBC models.
    Language English
    Publishing date 2020-08-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers12082209
    Database MEDical Literature Analysis and Retrieval System OnLINE

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