• Review of Korea Contents Association
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• v.12 no.3
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• pp.14-17
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• 2014

• Journal of the Korea Institute of Information and Communication Engineering
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• v.20 no.12
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• pp.2395-2400
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• 2016

Conventional drug carriers such as liposomes, nanoparticles, polymer micelles, polymeric conjugate and lipid microemulsion for cancer chemotherapy shield normal tissues from toxic drugs to treat cancer cells in tumors. However, inaccurate tumor targeting uncontrolled drug release from the carriers and unwanted accumulation in healthy sites can limit treatment efficacy with current conventional drug carriers with insufficient concentrations of drugs in the tumors and unexpected side effects as a result. Sickle red blood cells show natural tumor preferential accumulation without any manipulation due to the adhesive interaction between molecular receptors on the membrane surface and counter-receptor on endothelial cells. In addition, structural changes of microvascular in tumor sites enhances polymerization of sickle red blood cells. In this research, we examined the use of sickle red blood cells as a new drug carrier with novel tumor targeting and controlled release properties to quantify its therapeutic effects.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2016.05a
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• pp.715-717
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• 2016

Conventional drug carriers such as liposomes, nanoparticles, polymer micelles, polymeric conjugate and lipid microemulsion for cancer chemotherapy shield normal tissues from toxic drugs to treat cancer cells in tumors. However, inaccurate tumor targeting uncontrolled drug release from the carriers and unwanted accumulation in healthy sites can limit treatment efficacy with current conventional drug carriers with insufficient concentrations of drugs in the tumors and unexpected side effects as a result. In this research, we examined the use of sickle red blood cells as a new drug carrier with novel tumor targeting and controlled release properties. Sickle red blood cells show natural tumor preferential accumulation without any manipulation and controlled drug release is possible using a hemolysis method with photosensitizers.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2015.10a
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• pp.958-960
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• 2015

Sickle cells possess a unique combination of traits that may enable their use as models for novel synthetic tumor targeting controlled release drug carriers with the ability to treat disseminated tumors in advanced metastatic disease. In this study, we assess the ability of light-activated release sickle cells to enhance tumor delivery of the fluorescent dye calcein by delayed photolysis controlled release compared to free systemic administration of calcein. Sickle cells from mouse models of the disease were shown to preferentially accumulate in tumors compared to adjacent tissue, in 4T1 tumors in mice on a time scale about 12 hours. Sickle cells photosensitized with protoporphyrin IX achieved delayed release of 50% of contents 8-16 hours after photoactivation, which was deemed useful for in vivo delivery of cargo to tumors given the tumor accumulation time of the sickle cells. Sickle cells may be useful as a model for new synthetic drug carrier particles with delayed photolysis controlled release properties.

• KSBB Journal
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• v.22 no.5
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• pp.318-321
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• 2007

Photodynamic therapy (PDT) is a targeted-tumor treatment system using a photosensitizer, light and oxygen to treat malignant tumor. We have investigated the cytotoxicity of 4 types of phthalocyanine derivative (silver phthalocyanine, iron (III) phthalocyanine, copper (II) phthalocyanine, nickel (II) phthalocyanine) against lung and breast cancers based on photodynamic therapy. As a result, phthalocyanine derivatives indicated a higher anticancer activity on a breast cancer cell line. Among the tested phthalocyanines, silver phthalocyanine (AgPc) showed a lower cytotoxicity against a normal cell line. In addition AgPc gave a good color characteristic when it is solubilized in water. Finally AgPc was selected as a potential antitumor agent for breast cancer.

• Journal of Food Hygiene and Safety
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• v.28 no.3
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• pp.202-206
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• 2013

High-grade mucoepidermoid carcinomas (MECs) have difficulty in cure and 5-year survival rate is quiet low. Therefore, we need new therapeutic agents and molecular targets. Betulinic acid (BA) is one of the materials which is easily found in the world and shows tumor-suppress effects in various tumor types. In addition, many kinds of normal tissues have a resistance to BA treatment. In this study, we investigated the anti-proliferative activity of BA and its molecular targets in MC-3 human MEC cells using western blot analysis and DAPI staining. BA inhibited cell viability and induced apoptosis in MC-3 cells. It affected Specificity protein 1 (Sp1) and its downstream molecule, survivin whereas it did not affect myeloid cell leukemia-1 (Mcl-1). Therefore, we suggest that BA can be a potential anti-cancer drug candidate regulating Sp 1 and survivin to exert apoptotic cell death.

• Journal of Life Science
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• v.29 no.1
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• pp.105-111
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• 2019

In recent years, progress has been made in the search for the development of new anti-cancer agents by employing specific inhibitors of histone deacetylase (HDAC)-6 to block signal transduction pathways in cancer cells. This study examined the effects of tubastatin A (TubA), an HDAC-6 inhibitor, on the growth and development of immature oocytes in murine ovaries using RNA sequencing analysis. The results from a gene set enrichment analysis (GSEA) indicated that the expression of most of the gene sets involved in the cell cycle and control and progression of meiosis decreased in the TubA-treated group as compared with that in germinal vesicle (GV) stage oocytes. In addition, an ingenuity pathway analysis (IPA) suggested that TubA not only caused increased expression of p53 and pRB and decreased expression of CDK4/6 and cyclin D but also caused elevated expression of genes involved in the control of the DNA check point in G2/M stage oocytes. These results suggest that TubA may induce cell cycle arrest and apoptosis through the induction of changes in the expression of genes involved in signal transduction pathways associated with DNA damage and the cell cycle of immature oocytes in the ovary.

• Journal of Life Science
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• v.17 no.6 s.86
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• pp.748-755
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• 2007

The in vitro activity of ST1571, an inhibitor of the Abl group of protein-tyrosine kinases, alone or in combination with camptothecin (CPT), a specific topoisomerase I inhibitor, was evaluated against human cancer cells with different metastatic capacity and drug resistance potency. These cell lines showed different sensitivity to ST157 on growth inhibition, and the expression of DNA-dependent protein kinase (DNA-PK), which interacts constitutively with c-Abl, was significantly decreased in drug sensitive CEM and MCF-7 cells and poorly metastatic PC3 and KMl2 cells as compared with that of multidrug resistant CEM/MDR and MCF-7/MDR cells and highly metastatic PC3-MM2 and KM/L4a cells, respectively. These results suggest differential modulation of DNA-PK by ST1571 treatment in drug resistance and metastatic degree dependent manner. We showed that CPT as well as ST1571 significantly inhibits the expression of DNA-PK. The combined treatment with ST15fl and CPT revealed synergistic effect, and the effect was accompanied by inhibition of cell proliferation due to significant reduced expression of DNA-PK components, which resulted in CPT sensitizes human cancer cells resistant to ST1571. Therefore, the results of our study suggested that the suppression of DNA-PK using combination of ST1571 and CPT could be a novel molecular target for against drugresistant and metastatic cancer cells.

• Journal of Life Science
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• v.29 no.4
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• pp.499-508
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• 2019

Cancer stem cells (CSCs), which are primarily responsible for metastasis and recurrence, have self-renewal, differentiation, therapeutic resistance, and tumor formation abilities. Numerous studies have demonstrated the signaling pathways essential for the acquisition and maintenance of CSC characteristics, such as WNT/${\beta}$-catenin, Hedgehog, Notch, B lymphoma Mo-MLV insertion region 1 homolog (BMI1), Bone morphogenetic protein (BMP), and TGF-${\beta}$ signals. However, few therapeutic strategies have been developed that can selectively eliminate CSCs. Recently, neutralizing antibodies against Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and Programmed cell death protein 1 (PD-1)/Programmed death-ligand 1 (PD-L1), immune checkpoint inhibitors (ICIs), have shown promising outcomes in clinical trials of melanoma, lung cancer, and pancreatic cancer, as well as in hematologic malignancies. ICIs are considered to outperform conventional anticancer drugs by maintaining long-lasting anti-cancer effects, with less severe side effects. Several studies reported that ICIs successfully blocked CSC properties in head and neck squamous carcinomas, melanomas, and breast cancer. Together, these findings suggest that novel and effective anticancer therapeutic modalities using ICIs for selective elimination of CSCs may be developed in the near future. In this review, we highlight the origin and characteristics of CSCs, together with critical signaling pathways. We also describe progress in ICI-mediated anticancer treatment to date and present perspectives on the development of CSC-targeting ICIs.

• Radiation Oncology Journal
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• v.22 no.2
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• pp.77-90
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• 2004

Purpose: The purpose of this review Is to provide an update on novel radiation treatments for head and neck cancer Recent Findings: Despite the remarkable advances In chemotherapy and radiotherapy techniques, the management of advanced head and neck cancer remains challenging. Epidermal growth factor receptor (EGFR) Is an appealing target for novel therapies In head and neck cancer because not only EGFR activation stimulates many important signaling pathways associated with cancer development and progression, and importantly, resistance to radiation. Furthermore, EGFR overexpression Is known to be portended for a worse outcome in patients with advanced head and neck cancer. Two categories of compounds designed to abrogate EGFR signaling, such as monoclonal antibodies (Cetuxlmab) and tyrosine kinase inhibitors (ZD1839 and 051-774) have been assessed and have been most extensively studied In preclinical models and clinical trials. Additional TKIs In clinical trials include a reversible agent, Cl-1033, which blocks activation of all erbB receptors. Encouraging preclinical data for head and neck cancers resulted In rapid translation Into the clinic. Results from Initial clinical trials show rather surprisingly that only minority of patients benefited from EGFR inhibition as monotherapy or In combination with chemotherapy. In this review, we begin with a brief summary of erbB- mediated signal transduction. Subsequently, we present data on prognostic-predictive value of erbB receptor expression in HNC followed by preclinlcal and clinical data on the role of EGFR antagonists alone or in combination with radiation In the treatment of HNC. Finally, we discuss the emerging thoughts on resistance to EGFR biockade and efforts In the development of multiple-targeted therapy for combination with chemotherapy or radiation. Current challenges for investigators are to determine (1 ) who will benefit from targeted agents and which agents are most appropriate to combine with radiation and/or chemotherapy, (2) how to sequence these agents with radiation and/or cytotoxlc compounds, (3) reliable markers for patient selection and verification of effective blockade of signaling in vivo, and (4) mechanisms behind intrinsic or acquired resistance to targeted agents to facilitate rational development of multi-targeted therapy, Other molecuiar-targeted approaches In head and neck cancer were briefly described, Including angloenesis Inhibitors, farnesyl transferase inhibitors, cell cycle regulators, and gene therapy Summary: Novel targeted theraples are highly appealing in advanced head and neck cancer, and the most premising strategy to use them Is a matter of intense Investigation.