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Article ; Online: Combination Treatment Strategies to Overcome PARP Inhibitor Resistance.

Soung, Young-Hwa / Chung, Jun

2023 Volume 13, Issue 10

Abstract: Poly(ADP-ribose) polymerase (PARP) enzymes have been shown to be essential for DNA repair pathways, including homologous recombination repair (HRR). Cancers with HRR defects (e.g., BRCA1 and BRCA2 mutations) are targets for PARP inhibitors (PARPis) based ...

Abstract	Poly(ADP-ribose) polymerase (PARP) enzymes have been shown to be essential for DNA repair pathways, including homologous recombination repair (HRR). Cancers with HRR defects (e.g., BRCA1 and BRCA2 mutations) are targets for PARP inhibitors (PARPis) based on the exploitation of "synthetic lethality". As a result, PARPis offer a promising treatment option for advanced ovarian and breast cancers with deficiencies in HRR. However, acquired resistance to PARPis has been reported for most tumors, and not all patients with BRCA1/2 mutations respond to PARPis. Therefore, the formulation of effective treatment strategies to overcome resistance to PARPis is urgently necessary. This review summarizes the molecular mechanism of therapeutic action and resistance to PARPis, in addition to emerging combination treatment options involving PARPis.
MeSH term(s)	Female ; Humans ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use ; BRCA1 Protein/genetics ; BRCA1 Protein/metabolism ; Ovarian Neoplasms/genetics ; BRCA2 Protein/genetics ; Antineoplastic Agents/therapeutic use ; Poly(ADP-ribose) Polymerases/metabolism
Chemical Substances	Poly(ADP-ribose) Polymerase Inhibitors ; BRCA1 protein, human ; BRCA1 Protein ; BRCA2 protein, human ; BRCA2 Protein ; Antineoplastic Agents ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
Language	English
Publishing date	2023-10-03
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13101480
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Sensitization of Triple-Negative Breast Cancers to Poly ADP Ribose Polymerase Inhibition Independent of BRCA1/2 Mutation Status by Chemically Modified microRNA-489.

Soung, Young Hwa / Ju, Jingfang / Chung, Jun

Cells

2023 Volume 13, Issue 1

Abstract: Chemoresistance and inefficient therapeutic efficacies in triple-negative breast cancers (TNBCs) are among the major clinical problems in breast cancers. A potential new method to sensitize these tumors to current treatment options is, therefore, urgent ... ...

Abstract	Chemoresistance and inefficient therapeutic efficacies in triple-negative breast cancers (TNBCs) are among the major clinical problems in breast cancers. A potential new method to sensitize these tumors to current treatment options is, therefore, urgent and necessary. Our previous studies demonstrated that miR-489 serves as one of the top tumor-suppressing miRs and features downregulated expression in metastatic TNBCs and that the restoration of miR-489 expression in TNBCs effectively inhibits the metastatic potentials of TNBCs both in vitro and in vivo. The chemical modification of miR-489 (CMM489) through the replacement of uracil with 5-FU further enhances the therapeutic potential of miR-489. In the present study, we tested the effects of CMM489 in synergizing DNA damage response (DDR) inhibitors such as PARP inhibitors. CMM489 is particularly effective in sensitizing TNBC cell lines with inherent resistance to PARP inhibitors regardless of BRCA mutation status. One of the anti-cancer mechanisms through which CMM489 synergizes with PARP inhibitors is the blockade of homologous recombination (HR) in TNBC cells upon DNA damage. The results of this study highlight the potential use of CMM489 in combination treatments with PARP inhibitors in TNBCs.
MeSH term(s)	Humans ; Poly(ADP-ribose) Polymerases ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; BRCA1 Protein/genetics ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; BRCA2 Protein/genetics ; MicroRNAs/genetics ; Mutation/genetics
Chemical Substances	Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; BRCA1 protein, human ; BRCA1 Protein ; Poly(ADP-ribose) Polymerase Inhibitors ; BRCA2 protein, human ; BRCA2 Protein ; MicroRNAs ; MIRN489 microRNA, human
Language	English
Publishing date	2023-12-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13010049
Database	MEDical Literature Analysis and Retrieval System OnLINE

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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
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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
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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
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Article: Exosomes in Cancer Diagnostics.

Soung, Young Hwa / Ford, Shane / Zhang, Vincent / Chung, Jun

Cancers

2017 Volume 9, Issue 1

Abstract: Exosomes are endosome derived extracellular vesicles of 30-120 nm size ranges. Exosomes have been identified as mediators of cell-to-cell communication by transferring bioactive molecules such as nucleic acids, proteins and lipids into recipient cells. ... ...

Abstract	Exosomes are endosome derived extracellular vesicles of 30-120 nm size ranges. Exosomes have been identified as mediators of cell-to-cell communication by transferring bioactive molecules such as nucleic acids, proteins and lipids into recipient cells. While exosomes are secreted by multiple cell types, cancer derived exosomes not only influence the invasive potentials of proximally located cells, but also affect distantly located tissues. Based on their ability to alter tumor microenvironment by regulating immunity, angiogenesis and metastasis, there has been growing interest in defining the clinical relevance of exosomes in cancers. In particular, exosomes are valuable sources for biomarkers due to selective cargo loading and resemblance to their parental cells. In this review, we summarize the recent findings to utilize exosomes as cancer biomarkers for early detection, diagnosis and therapy selection.
Language	English
Publishing date	2017-01-12
Publishing country	Switzerland
Document type	Review ; Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers9010008
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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
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Article ; Online: Arrestin Domain Containing 3 Reverses Epithelial to Mesenchymal Transition and Chemo-Resistance of TNBC Cells by Up-Regulating Expression of miR-200b

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

Cells, Vol 8, Iss 7, p

2019 Volume 692

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.
Keywords	ARRDC3 ; miR-200b ; 5-fluorourancil (5-FU) ; epithelial to mesenchymal transition (EMT) ; chemo-resistance ; triple negative breast cancer (TNBC) ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2019-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Exosomes in Cancer Diagnostics

Young Hwa Soung / Shane Ford / Vincent Zhang / Jun Chung

Cancers, Vol 9, Iss 1, p

2017 Volume 8

Abstract: Exosomes are endosome derived extracellular vesicles of 30–120 nm size ranges. Exosomes have been identified as mediators of cell-to-cell communication by transferring bioactive molecules such as nucleic acids, proteins and lipids into recipient cells. ... ...

Abstract	Exosomes are endosome derived extracellular vesicles of 30–120 nm size ranges. Exosomes have been identified as mediators of cell-to-cell communication by transferring bioactive molecules such as nucleic acids, proteins and lipids into recipient cells. While exosomes are secreted by multiple cell types, cancer derived exosomes not only influence the invasive potentials of proximally located cells, but also affect distantly located tissues. Based on their ability to alter tumor microenvironment by regulating immunity, angiogenesis and metastasis, there has been growing interest in defining the clinical relevance of exosomes in cancers. In particular, exosomes are valuable sources for biomarkers due to selective cargo loading and resemblance to their parental cells. In this review, we summarize the recent findings to utilize exosomes as cancer biomarkers for early detection, diagnosis and therapy selection.
Keywords	exosomes ; cancer ; biomarkers ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R
Subject code	610
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Curcumin inhibition of the functional interaction between integrin α6β4 and the epidermal growth factor receptor.

Soung, Young Hwa / Chung, Jun

Molecular cancer therapeutics

2011 Volume 10, Issue 5, Page(s) 883–891

Abstract: The functional interaction between integrin α6β4 and growth factor receptors has been implicated in key signaling pathways important for cancer cell function. However, few attempts have been made to selectively target this interaction for therapeutic ... ...

Abstract	The functional interaction between integrin α6β4 and growth factor receptors has been implicated in key signaling pathways important for cancer cell function. However, few attempts have been made to selectively target this interaction for therapeutic intervention. Previous studies showed that curcumin, a yellow pigment isolated from turmeric, inhibits integrin α6β4 signaling important for breast carcinoma cell motility and invasion, but the mechanism is not currently known. To address this issue, we tested the hypothesis that curcumin inhibits the functional interaction between α6β4 and the epidermal growth factor receptor (EGFR). In this study, we found that curcumin disrupts functional and physical interactions between α6β4 and EGFR, and blocks α6β4/EGFR-dependent functions of carcinoma cells expressing the signaling competent form of α6β4. We further showed that curcumin inhibits EGF-dependent mobilization of α6β4 from hemidesmosomes to the leading edges of migrating cells such as lammelipodia and filopodia, and thereby prevents α6β4 distribution to lipid rafts where functional interactions between α6β4 and EGFR occur. These data suggest a novel paradigm in which curcumin inhibits α6β4 signaling and functions by altering intracellular localization of α6β4, thus preventing its association with signaling receptors such as EGFR.
MeSH term(s)	Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Carcinoma/metabolism ; Cell Line, Tumor ; Curcumin/chemistry ; Curcumin/pharmacology ; Epidermal Growth Factor/metabolism ; ErbB Receptors/antagonists & inhibitors ; ErbB Receptors/metabolism ; Hemidesmosomes/metabolism ; Humans ; Integrin alpha6beta4/antagonists & inhibitors ; Integrin alpha6beta4/metabolism ; Membrane Microdomains/drug effects ; Membrane Microdomains/metabolism ; Protein Binding/drug effects ; Protein Transport/drug effects ; Pseudopodia/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Integrin alpha6beta4 ; Epidermal Growth Factor (62229-50-9) ; ErbB Receptors (EC 2.7.10.1) ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2011-03-09
Publishing country	United States
Document type	Journal Article ; 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-10-1053
Database	MEDical Literature Analysis and Retrieval System OnLINE

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