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Article ; Online: MiRNA10b-directed nanotherapy effectively targets brain metastases from breast cancer.

Yoo, Byunghee / Ross, Alana / Pantazopoulos, Pamela / Medarova, Zdravka

2021 Volume 11, Issue 1, Page(s) 2844

Abstract: RNA interference represents one of the most appealing therapeutic modalities for cancer because of its potency, versatility, and modularity. Because the mechanism is catalytic and affects the expression of disease-causing antigens at the post- ... ...

Abstract	RNA interference represents one of the most appealing therapeutic modalities for cancer because of its potency, versatility, and modularity. Because the mechanism is catalytic and affects the expression of disease-causing antigens at the post-transcriptional level, only small amounts of therapeutic need to be delivered to the target in order to exert a robust therapeutic effect. RNA interference is also advantageous over other treatment modalities, such as monoclonal antibodies or small molecules, because it has a much broader array of druggable targets. Finally, the complementarity of the genetic code gives us the opportunity to design RNAi therapeutics using computational, rational approaches. Previously, we developed and tested an RNAi-targeted therapeutic, termed MN-anti-miR10b, which was designed to inhibit the critical driver of metastasis and metastatic colonization, miRNA-10b. We showed in animal models of metastatic breast cancer that MN-anti-miR10b accumulated into tumors and metastases in the lymph nodes, lungs, and bone, following simple intravenous injection. We also found that treatment incorporating MN-anti-miR10b was effective at inhibiting the emergence of metastases and could regress already established metastases in the lymph nodes, lungs, and bone. In the present study, we extend the application of MN-anti-miR10b to a model of breast cancer metastatic to the brain. We demonstrate delivery to the metastatic lesions and obtain evidence of a therapeutic effect manifested as inhibition of metastatic progression. This investigation represents an additional step towards translating similar RNAi-targeted therapeutics for the systemic treatment of metastatic disease.
MeSH term(s)	Animals ; Brain Neoplasms/genetics ; Brain Neoplasms/secondary ; Brain Neoplasms/therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Cell Line, Tumor ; Cell Proliferation/genetics ; Female ; Humans ; Mice ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/genetics ; RNA Interference ; RNAi Therapeutics/methods ; Xenograft Model Antitumor Assays
Chemical Substances	MIRN10 microRNA, human ; MicroRNAs
Language	English
Publishing date	2021-02-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-82528-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: MiRNA10b-directed nanotherapy effectively targets brain metastases from breast cancer

Byunghee Yoo / Alana Ross / Pamela Pantazopoulos / Zdravka Medarova

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 7

Abstract: Abstract RNA interference represents one of the most appealing therapeutic modalities for cancer because of its potency, versatility, and modularity. Because the mechanism is catalytic and affects the expression of disease-causing antigens at the post- ... ...

Abstract	Abstract RNA interference represents one of the most appealing therapeutic modalities for cancer because of its potency, versatility, and modularity. Because the mechanism is catalytic and affects the expression of disease-causing antigens at the post-transcriptional level, only small amounts of therapeutic need to be delivered to the target in order to exert a robust therapeutic effect. RNA interference is also advantageous over other treatment modalities, such as monoclonal antibodies or small molecules, because it has a much broader array of druggable targets. Finally, the complementarity of the genetic code gives us the opportunity to design RNAi therapeutics using computational, rational approaches. Previously, we developed and tested an RNAi-targeted therapeutic, termed MN-anti-miR10b, which was designed to inhibit the critical driver of metastasis and metastatic colonization, miRNA-10b. We showed in animal models of metastatic breast cancer that MN-anti-miR10b accumulated into tumors and metastases in the lymph nodes, lungs, and bone, following simple intravenous injection. We also found that treatment incorporating MN-anti-miR10b was effective at inhibiting the emergence of metastases and could regress already established metastases in the lymph nodes, lungs, and bone. In the present study, we extend the application of MN-anti-miR10b to a model of breast cancer metastatic to the brain. We demonstrate delivery to the metastatic lesions and obtain evidence of a therapeutic effect manifested as inhibition of metastatic progression. This investigation represents an additional step towards translating similar RNAi-targeted therapeutics for the systemic treatment of metastatic disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article: Clinical Applications of Short Non-Coding RNA-Based Therapies in the Era of Precision Medicine.

Smith, Ellen S / Whitty, Eric / Yoo, Byunghee / Moore, Anna / Sempere, Lorenzo F / Medarova, Zdravka

Cancers

2022 Volume 14, Issue 6

Abstract: Traditional targeted therapeutic agents have relied on small synthetic molecules or large proteins, such as monoclonal antibodies. These agents leave a lot of therapeutic targets undruggable because of the lack or inaccessibility of active sites and/or ... ...

Abstract	Traditional targeted therapeutic agents have relied on small synthetic molecules or large proteins, such as monoclonal antibodies. These agents leave a lot of therapeutic targets undruggable because of the lack or inaccessibility of active sites and/or pockets in their three-dimensional structure that can be chemically engaged. RNA presents an attractive, transformative opportunity to reach any genetic target with therapeutic intent. RNA therapeutic design is amenable to modularity and tunability and is based on a computational blueprint presented by the genetic code. Here, we will focus on short non-coding RNAs (sncRNAs) as a promising therapeutic modality because of their potency and versatility. We review recent progress towards clinical application of small interfering RNAs (siRNAs) for single-target therapy and microRNA (miRNA) activity modulators for multi-target therapy. siRNAs derive their potency from the fact that the underlying RNA interference (RNAi) mechanism is catalytic and reliant on post-transcriptional mRNA degradation. Therapeutic siRNAs can be designed against virtually any mRNA sequence in the transcriptome and specifically target a disease-causing mRNA variant. Two main classes of microRNA activity modulators exist to increase (miRNA mimics) or decrease (anti-miRNA inhibitors) the function of a specific microRNA. Since a single microRNA regulates the expression of multiple target genes, a miRNA activity modulator can have a more profound effect on global gene expression and protein output than siRNAs do. Both types of sncRNA-based drugs have been investigated in clinical trials and some siRNAs have already been granted FDA approval for the treatment of genetic, cardiometabolic, and infectious diseases. Here, we detail clinical results using siRNA and miRNA therapeutics and present an outlook for the potential of these sncRNAs in medicine.
Language	English
Publishing date	2022-03-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14061588
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Article ; Online: Screening of potential miRNA therapeutics for the prevention of multi-drug resistance in cancer cells.

Medarova, Zdravka / Pantazopoulos, Pamela / Yoo, Byunghee

Scientific reports

2020 Volume 10, Issue 1, Page(s) 1970

Abstract: Chemotherapy, a major cancer treatment approach, suffers seriously from multidrug resistance (MDR), generally caused by innate DNA repair proteins that reverse the DNA modification by anti-cancer therapeutics or trans-membrane efflux proteins that pump ... ...

Abstract	Chemotherapy, a major cancer treatment approach, suffers seriously from multidrug resistance (MDR), generally caused by innate DNA repair proteins that reverse the DNA modification by anti-cancer therapeutics or trans-membrane efflux proteins that pump anti-cancer therapeutics out of the cytosol. This project focused on finding microRNAs that can regulate MDR proteins by managing corresponding mRNA levels through post-transcriptional regulation based on nucleotide sequence matching. Screening was done with bioinformatics databases for unpublished/unexplored microRNAs with high nucleotide sequence correspondence to two representative MDR proteins, MGMT (a DNA repair protein) and ABCB1 (an efflux protein), revealing microRNA-4539 and microRNA-4261 respectively. To investigate the enhancement of chemotherapeutics in cancer cells, high MGMT expressing glioblastoma (T98G) and a high ABCB1 expressing triple-negative breast cancer cell line (MDA-MB-231-luc) were treated with varying concentrations of chemotherapeutics and corresponding miRNAs. Newly identified MDR-related miRNAs (MDRmiRs) enhanced the response to anti-cancer therapeutics and resulted in effective cell death. In this study, we demonstrated that therapeutic miRNAs could be identified based on the nucleotide sequence matching of miRNAs to targeted mRNA and the same approach could be employed for the screening of therapeutic candidates to regulate specific target proteins in diverse diseases.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B/antagonists & inhibitors ; ATP Binding Cassette Transporter, Subfamily B/metabolism ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Computational Biology ; DNA Repair/drug effects ; Drug Resistance, Multiple/genetics ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; Drug Screening Assays, Antitumor ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; MicroRNAs/analysis ; MicroRNAs/genetics ; Neoplasms/drug therapy ; Neoplasms/genetics ; Oligonucleotides/genetics ; Oligonucleotides/pharmacology ; Oligonucleotides/therapeutic use
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B ; MicroRNAs ; Oligonucleotides
Language	English
Publishing date	2020-02-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-58919-2
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Article ; Online: Forkhead box protein D2 suppresses colorectal cancer by reprogramming enhancer interactions.

Kim, Hyo-Min / Kang, Byunghee / Park, Sohyun / Park, Hyorim / Kim, Chan Johng / Lee, Hyeonji / Yoo, Mijoung / Kweon, Mi-Na / Im, Sin-Hyeog / Kim, Tae Il / Roh, Tae-Young

Nucleic acids research

2023 Volume 51, Issue 12, Page(s) 6143–6155

Abstract: Somatic stem cells contribute to normal tissue homeostasis, and their epigenomic features play an important role in regulating tissue identities or developing disease states. Enhancers are one of the key players controlling chromatin context-specific ... ...

Abstract	Somatic stem cells contribute to normal tissue homeostasis, and their epigenomic features play an important role in regulating tissue identities or developing disease states. Enhancers are one of the key players controlling chromatin context-specific gene expression in a spatial and temporal manner while maintaining tissue homeostasis, and their dysregulation leads to tumorigenesis. Here, epigenomic and transcriptomic analyses reveal that forkhead box protein D2 (FOXD2) is a hub for the gene regulatory network exclusive to large intestinal stem cells, and its overexpression plays a significant role in colon cancer regression. FOXD2 is positioned at the closed chromatin and facilitates mixed-lineage leukemia protein-4 (MLL4/KMT2D) binding to deposit H3K4 monomethylation. De novo FOXD2-mediated chromatin interactions rewire the regulation of p53-responsive genes and induction of apoptosis. Taken together, our findings illustrate the novel mechanistic details of FOXD2 in suppressing colorectal cancer growth and suggest its function as a chromatin-tuning factor and a potential therapeutic target for colorectal cancer.
MeSH term(s)	Humans ; Chromatin/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Enhancer Elements, Genetic ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Histones/genetics ; Histones/metabolism
Chemical Substances	Chromatin ; Forkhead Transcription Factors ; Histones ; FOXD2 protein, human
Language	English
Publishing date	2023-05-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad361
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Article: New Directions in the Study and Treatment of Metastatic Cancer.

Yoo, Byunghee / Fuchs, Bryan C / Medarova, Zdravka

Frontiers in oncology

2018 Volume 8, Page(s) 258

Abstract: Traditional cancer therapy has relied on a strictly cytotoxic approach that views non-metastatic and metastatic tumor cells as identical in terms of molecular biology and sensitivity to therapeutic intervention. Mounting evidence suggests that, in fact, ... ...

Abstract	Traditional cancer therapy has relied on a strictly cytotoxic approach that views non-metastatic and metastatic tumor cells as identical in terms of molecular biology and sensitivity to therapeutic intervention. Mounting evidence suggests that, in fact, non-metastatic and metastatic tumor cells differ in key characteristics that could explain the capacity of the metastatic cells to not only escape the primary organ but also to survive while in the circulation and to colonize a distant organ. Here, we lay out a framework for a new multi-pronged therapeutic approach. This approach involves modifying the local microenvironment of the primary tumor to inhibit the formation and release of metastatic cells; normalizing the microenvironment of the metastatic organ to limit the capacity of metastatic tumor cells to invade and colonize the organ; remediating the immune response to tumor neoantigens; and targeting metastatic tumor cells on a systemic level by restoring critical and unique aspects of the cell's phenotype, such as anchorage dependence. Given the limited progress against metastatic cancer using traditional therapeutic strategies, the outlined paradigm could provide a more rational alternative to patients with metastatic cancer.
Language	English
Publishing date	2018-07-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00258
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Article: Case report: MicroRNA-10b as a therapeutic target in feline metastatic mammary carcinoma and its implications for human clinical trials.

Savan, N Anna / Saavedra, Paulo Vilar / Halim, Alan / Yuzbasiyan-Gurkan, Vilma / Wang, Ping / Yoo, Byunghee / Kiupel, Matti / Sempere, Lorenzo / Medarova, Zdravka / Moore, Anna

Frontiers in oncology

2022 Volume 12, Page(s) 959630

Abstract: Ninety percent of deaths from cancer are caused by metastasis. miRNAs are critical players in biological processes such as proliferation, metastasis, apoptosis, and self-renewal. We and others have previously demonstrated that miRNA-10b promotes ... ...

Abstract	Ninety percent of deaths from cancer are caused by metastasis. miRNAs are critical players in biological processes such as proliferation, metastasis, apoptosis, and self-renewal. We and others have previously demonstrated that miRNA-10b promotes metastatic cell migration and invasion. Importantly, we also showed that miR-10b is a critical driver of metastatic cell viability and proliferation. To treat established metastases by inhibiting miR-10b, we utilized a therapeutic, termed MN-anti-miR10b, composed of anti-miR-10b antagomirs, conjugated to iron oxide nanoparticles, that serve as delivery vehicles to tumor cells
Language	English
Publishing date	2022-10-26
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2022.959630
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Article: Radiolabeling and PET-MRI microdosing of the experimental cancer therapeutic, MN-anti-miR10b, demonstrates delivery to metastatic lesions in a murine model of metastatic breast cancer.

Le Fur, Mariane / Ross, Alana / Pantazopoulos, Pamela / Rotile, Nicholas / Zhou, Iris / Caravan, Peter / Medarova, Zdravka / Yoo, Byunghee

Cancer nanotechnology

2021 Volume 12, Issue 1

Abstract: Background: In our earlier work, we identified microRNA-10b (miR10b) as a master regulator of the viability of metastatic tumor cells. This knowledge allowed us to design a miR10b-targeted therapeutic consisting of anti-miR10b and ultrasmall iron oxide ... ...

Abstract	Background: In our earlier work, we identified microRNA-10b (miR10b) as a master regulator of the viability of metastatic tumor cells. This knowledge allowed us to design a miR10b-targeted therapeutic consisting of anti-miR10b and ultrasmall iron oxide magnetic nanoparticles (MN), termed MN-anti-miR10b. In mouse models of breast cancer, we demonstrated that MN-anti-miR10b caused durable regressions of established metastases with no evidence of systemic toxicity. As a first step towards translating MN-anti-miR10b for the treatment of metastatic breast cancer, we needed to determine if MN-anti-miR10b, which is so effective in mice, will also accumulate in human metastases. Results: In this study, we devised a method to efficiently radiolabel MN-anti-miR10b with Cu-64 ( Conclusion: Our results demonstrate that PET-MRI following a microdose injection of the agent will accurately reflect the innate biodistribution of the therapeutic. The tools developed in the present study lay the groundwork for the clinical testing of MN-anti-miR10b and other similar therapeutics in patients with cancer.
Language	English
Publishing date	2021-07-08
Publishing country	Austria
Document type	Journal Article
ISSN	1868-6958
ISSN	1868-6958
DOI	10.1186/s12645-021-00089-5
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Article: Guidelines for Rational Cancer Therapeutics.

Yoo, Byunghee / Billig, Ann-Marie / Medarova, Zdravka

Frontiers in oncology

2017 Volume 7, Page(s) 310

Abstract: Traditionally, cancer therapy has relied on surgery, radiation therapy, and chemotherapy. In recent years, these interventions have become increasingly replaced or complemented by more targeted approaches that are informed by a deeper understanding of ... ...

Abstract	Traditionally, cancer therapy has relied on surgery, radiation therapy, and chemotherapy. In recent years, these interventions have become increasingly replaced or complemented by more targeted approaches that are informed by a deeper understanding of the underlying biology. Still, the implementation of fully rational patient-specific drug design appears to be years away. Here, we present a vision of rational drug design for cancer that is defined by two major components: modularity and image guidance. We suggest that modularity can be achieved by combining a nanocarrier and an oligonucleotide component into the therapeutic. Image guidance can be incorporated into the nanocarrier component by labeling with a specific imaging reporter, such as a radionuclide or contrast agent for magnetic resonance imaging. While limited by the need for additional technological advancement in the areas of cancer biology, nanotechnology, and imaging, this vision for the future of cancer therapy can be used as a guide to future research endeavors.
Language	English
Publishing date	2017-12-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2017.00310
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Article ; Online: Lanthanide-mediated dephosphorylation used for peptide cleavage during solid phase peptide synthesis.

Yoo, Byunghee / Pagel, Mark D

Molecules (Basel, Switzerland)

2013 Volume 18, Issue 4, Page(s) 3894–3905

Abstract: Lanthanide(III) ions can accelerate the hydrolysis of phosphomonoesters and phosphodiesters in neutral aqueous solution. In this paper, lanthanide-mediated dephosphorylation has been applied in aqueous media as an orthogonal cleavage condition that can ... ...

Abstract	Lanthanide(III) ions can accelerate the hydrolysis of phosphomonoesters and phosphodiesters in neutral aqueous solution. In this paper, lanthanide-mediated dephosphorylation has been applied in aqueous media as an orthogonal cleavage condition that can be employed in conventional solid phase peptide synthesis (SPPS). A phosphorylated polymeric support for SPPS was developed using Boc chemistry. The cleavage of resin-bound phosphates was investigated with the addition of Eu(III), Yb(III), acid or base, a mixture of solvents or different temperatures. To demonstrate the utility of this approach for SPPS, a peptide sequence was synthesized on a phosphorylated polymeric support and quantitatively cleaved with lanthanide ions in neutral aqueous media. The protecting groups for side chains were retained during peptide cleavage using lanthanide ions. This new methodology provides a mild orthogonal cleavage condition of phosphoester as a linker during SPPS.
MeSH term(s)	Biopolymers/chemistry ; Hydrolysis ; Ions ; Lanthanoid Series Elements/chemistry ; Peptides/chemistry ; Phosphates/chemistry ; Phosphorylation ; Solid-Phase Synthesis Techniques/methods
Chemical Substances	Biopolymers ; Ions ; Lanthanoid Series Elements ; Peptides ; Phosphates
Language	English
Publishing date	2013-04-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules18043894
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