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Shilnikova Kristina,Piao Mei Jing,Kang Kyoung Ah,Fernando Pincha Devage Sameera Madushan,Herath Herath Mudiyanselage Udari Lakmini,Cho Suk Ju,Hyun Jin Won 한국응용약물학회 2022 Biomolecules & Therapeutics(구 응용약물학회지) Vol.30 No.2
Radiation resistance represents an imperative obstacle in the treatment of patients with colorectal cancer, which remains difficult to overcome. Here, we explored the anti-proliferative and migration-inhibiting properties of the natural product shikonin on a radiation- resistant human colon carcinoma cell line (SNU-C5RR). Shikonin reduced the viability of these cells in a dose-dependent manner; 38 μM of shikonin was determined as the half-maximal inhibitory concentration. Shikonin induced apoptotic cell death, as demonstrated by increased apoptotic body formation and the number of TUNEL-positive cells. Moreover, shikonin enhanced mitochondrial membrane depolarization and Bax expression and also decreased Bcl-2 expression with translocation of cytochrome c from mitochondria into the cytosol. In addition, shikonin activated mitogen-activated protein kinases, and their specific inhibitors reduced the cytotoxic effects of shikonin. Additionally, shikonin decreased the migration of SNU-C5RR cells via the upregulation of E-cadherin and downregulation of N-cadherin. Taken together, these results suggest that shikonin induces mitochondria-mediated apoptosis and attenuates epithelial-mesenchymal transition in SNU-C5RR cells.
Shilnikova, Kristina,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Park, Jeong Eon,Hyun, Yu Jae,Zhen, Ao Xuan,Jeong, Yong Joo,Jung, Uhee,Kim, In Gyu,Hyun, Jin Won D.A. Spandidos 2018 Oncology letters Vol.15 No.4
<P>Cisplatin-based chemotherapy often results in the development of chemoresistance when used to treat ovarian cancer, which is difficult to overcome. The present study investigated the cytotoxic and anti-migratory effects of shikonin, a naphthoquinone compound, on cisplatin-resistant human ovarian cancer A2780 cells (A2780-CR). Shikonin had a potent dose-dependent cytotoxic effect on A2780-CR cells, with 9 µM shikonin treatment reducing A2780-CR cell viability by 50%, validate using an MTT assay. Shikonin induced apoptosis, as evidenced by the increased number of apoptotic bodies, following staining with Hoechst 33342, and terminal deoxynucleotidyl cell transferase dUTP nick end labeling-positive cells following treatment. Flow cytometry and fluorescent microscope imaging, following JC-1 staining, revealed that shikonin increased mitochondrial membrane depolarization. Also it altered the levels of apoptosis-associated proteins, leading to diminished expression of B cell lymphoma-2 (Bcl-2), enhanced expression of Bcl-associated X, and cleavage of caspase-9 and −3, as revealed using western blot analysis. Shikonin activated mitogen-activated protein kinases; while treatment with specific inhibitors of these kinases attenuated the decline in cell viability induced by shikonin treatment. In addition, the cell migration assay and western blot analysis indicated that shikonin decreased the migratory capacity of A2780-CR cells via the upregulation of epithelial-cadherin and downregulation of neural-cadherin. Taken together, the results of the present study indicated that shikonin induces mitochondria-mediated apoptosis and attenuates the epithelial-mesenchymal transition in A2780-CR cells.</P>
Rui Zhang,박미경,Min Chang Oh,Jeong Eon Park,Kristina Shilnikova,Yu Jin Moon,Dong Hyun Kim,정우희,In Gyu Kim,현진원 대한암예방학회 2016 Journal of cancer prevention Vol.21 No.4
Background: Isoflavones are biologically active compounds that occur naturally in a variety of plants, with relatively high levels in soybean. Tectorigenin, an isoflavone, protects against hydrogen peroxide (H2O2)-induced cell damage. However, the underlying mechanism is unknown. Methods: The MTT assay was performed to determine cell viability. Catalase activity was assessed by determining the amount of enzyme required to degrade 1 μM H2O2. Protein expression of catalase, phospho-extracellular signal-regulated kinase (ERK), IκB-α, and NF-κB were evaluated by Western blot analysis. A mobility shift assay was performed to assess the DNA-binding ability of NF-κB. Transient transfection and a NF-κB luciferase assay were performed to assess transcriptional activity. Results: Tectorigenin reduced H2O2-induced death of Chinese hamster lung fibroblasts (V79-4). In addition, tectorigenin increased the activity and protein expression of catalase. Blockade of catalase activity attenuated the protective effect of tectorigenin against oxidative stress. Furthermore, tectorigenin enhanced phosphorylation of ERK and nuclear expression of NF-B, while inhibition of ERK and NF-κB attenuated the protective effect of tectorigenin against oxidative stress. Conclusions: Tectorigenin protects cells against oxidative damage by activating catalase and modulating the ERK and NF-κB signaling pathway.
( Jeong Eon Park ),( Mei Jing Piao ),( Kyoung Ah Kang ),( Kristina Shilnikova ),( Yu Jae Hyun ),( Sei Kwan Oh ),( Yong Joo Jeong ),( Sungwook Chae ),( Jin Won Hyun ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.4
Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an IC50 value of 6 μM JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells.
Park, Jeong Eon,Piao, Mei Jing,Kang, Kyoung Ah,Shilnikova, Kristina,Hyun, Yu Jae,Oh, Sei Kwan,Jeong, Yong Joo,Chae, Sungwook,Hyun, Jin Won The Korean Society of Applied Pharmacology 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.4
Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an $IC_{50}$ value of $6{\mu}M$ JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells.
Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
Kang, Kyoung Ah,Piao, Mei Jing,Ryu, Yea Seong,Hyun, Yu Jae,Park, Jeong Eon,Shilnikova, Kristina,Zhen, Ao Xuan,Kang, Hee Kyoung,Koh, Young Sang,Jeong, Yong Joo,Hyun, Jin Won Spandidos Publications 2017 International journal of oncology Vol.51 No.4
<P>The present study determined whether luteolin induces HT-29 colon cancer cell death through an antioxidant effect such as the activation of antioxidant enzymes. Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC). Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells. Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol, and increased the levels of the active forms of caspase-9 and caspase-3. Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells. Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis. The apoptotic effect of luteolin was mediated by the activation of the mitogen-activated protein kinase signaling pathway. The present results indicate that luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.</P>
Park, Jeong Eon,Hyun, Yu Jae,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Shilnikova, Kristina,Zhen, Ao Xuan,Ahn, Mee Jung,Ahn, Yong Seok,Koh, Young Sang,Kang, Hee Kyoung,Hyun, Jin Won Elsevier 2018 Journal of Functional Foods Vol.46 No.-
<P><B>Abstract</B></P> <P>This study investigated the protective effect of mackerel-derived fermented fish oil (FFO) against UVB radiation-induced oxidative stress in human HaCaT keratinocytes and mouse skin tissue. FFO treatment scavenged UVB-induced intracellular reactive oxygen species and attenuated oxidative modifications including lipid peroxidation, protein carbonylation, and DNA damage. FFO treatment reduced UVB-induced apoptosis by reducing DNA fragmentation, caspase activation, and proapoptotic protein expression. UVB radiation activated phospho-extracellular signal-regulated kinase, phospho-c-Jun N-terminal kinase, and phospho-p38, whereas their specific inhibitors with FFO treatment abrogated the cell viability and apoptosis increased by UVB irradiation. FFO was more cytoprotective than docosahexaenoic acid, the main component of fish oil, against UVB exposure. Furthermore, the cytoprotective effect of FFO was evident in both UVB-exposed HaCaT cell and mouse models. Overall, these results demonstrate that FFO protects the skin against UVB-induced oxidative stress through antioxidant effects. FFO has the potential for development as a functional food against UVB-induced skin damage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Mackerel-derived fermented fish oil (FFO) scavenged UVB-induced intracellular reactive oxygen species. </LI> <LI> FFO treatment attenuated UVB-induced oxidative skin cellular modifications and apoptotic cell death. </LI> <LI> FFO may be developed as a functional food against UVB-induced skin damage. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>FFO prevented epidermal damage including oxidative cellular damage and apoptotic cell death by directly inhibiting UVB radiation or decreasing ROS level induced by UVB radiation.</P> <P>[DISPLAY OMISSION]</P>
Susara Ruwan Kumara, Madduma Hewage,Piao, Mei Jing,Kang, Kyoung Ah,Ryu, Yea Seong,Park, Jeong Eon,Shilnikova, Kristina,Jo, Jin Oh,Mok, Young Sun,Shin, Jennifer H.,Park, Yeonsoo,Kim, Seong Bong,Yoo, Su NATIONAL HELLENIC RESEARCH FOUNDATION 2016 ONCOLOGY REPORTS Vol.36 No.4
<P>Colorectal cancer is a common type of tumor among both men and women worldwide. Conventional remedies such as chemotherapies pose the risk of side-effects, and in many cases cancer cells develop chemoresistance to these treatments. Non-thermal gas plasma (NTGP) was recently identified as a potential tool for cancer treatment. In this study, we investigated the potential use of NTGP to control SNUC5 human colon carcinoma cells. We hypothesized that NTGP would generate reactive oxygen species (ROS) in these cells, resulting in induction of endoplasmic reticulum (ER) stress. ROS generation, expression of ER stress-related proteins and mitochondrial calcium levels were analyzed. Our results confirmed that plasma-generated ROS induce apoptosis in SNUC5 cells. Furthermore, we found that plasma exposure resulted in mitochondrial calcium accumulation and expression of unfolded protein response (UPR) proteins such as glucose-related protein 78 (GRP78), protein kinase R (PKR)-like ER kinase (PERK), and inositol-requiring enzyme 1 (IRE1). Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway.</P>
Reduced Autophagy in 5-Fluorouracil Resistant Colon Cancer Cells
( Cheng Wen Yao ),( Kyoung Ah Kang ),( Mei Jing Piao ),( Yea Seong Ryu ),( Pattage Madushan Dilhara Jayatissa Fernando ),( Min Chang Oh ),( Jeong Eon Park ),( Kristina Shilnikova ),( Soo-young Na ),( 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.3
We investigated the role of autophagy in SNUC5/5-FUR, 5-fluorouracil (5-FU) resistant SNUC5 colon cancer cells. SNUC5/5- FUR cells exhibited low level of autophagy, as determined by light microscopy, confocal microscopy, and flow cytometry following acridine orange staining, and the decreased level of GFP-LC3 puncta. In addition, expression of critical autophagic proteins such as Atg5, Beclin-1 and LC3-II and autophagic flux was diminished in SNUC5/5-FUR cells. Whereas production of reactive oxygen species (ROS) was significantly elevated in SNUC5/5-FUR cells, treatment with the ROS inhibitor N-acetyl cysteine further reduced the level of autophagy. Taken together, these results indicate that decreased autophagy is linked to 5-FU resistance in SNUC5 colon cancer cells.
( Susara Ruwan Kumara Madduma Hewage ),( Mei Jing Piao ),( Kyoung Ah Kang ),( Yea Seong Ryu ),( Pattage Madushan Dilhara Jayatissa Fernando ),( Min Chang Oh ),( Jeong Eon Park ),( Kristina Shilnikova 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.4
Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKTNrf2, leading to elevated expression of GSH-synthesizing enzymes.