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Kim, Aeyung,Im, Minju,Ma, Jin Yeul Lychnia 2014 International journal of oncology Vol.45 No.5
<P>Anisi stellati fructus (ASF), commonly known as star anise, has long been used as a traditional Chinese medicine to treat inflammation, nervousness, insomnia and pain. In recent studies, it has been demonstrated that ASF possesses anti-bacterial, anti-fungal and anti-oxidant activities, as well as exhibits inhibitory effects on capillary?like tube formation in human umbilical vein endothelial cells (HUVECs). However, the effects of ASF extract on the metastatic potential of malignant tumor cells have not been examined. In this study, we found that daily oral administration of ASF (50 mg/kg) remarkably reduced the number of pulmonary metastatic colonies of B16F10 cells in C57BL/6J mice with no observed systemic toxicity. In an in vitro system, ASF inhibited metastatic properties, including anchorage?independent colony formation, migration and invasion. Upon phorbol 12-myristate 13-acetate (PMA) stimulation, the mRNA levels of matrix metalloproteinases (MMPs) -9, -13, -14 and urokinase plasminogen activator (uPA) decreased in a dose-dependent manner with ASF treatment. Gelatinase, type I collagenase, and uPA activities were also suppressed efficiently by ASF treatment. In response to PMA, NF-κB and AP-1 activation as well as p38 phosphorylation, which are crucial for MMP activation, were significantly decreased by ASF. In particular, ASF considerably inhibited tumor-induced HUVEC migration and tube formation and suppressed in vivo tumor-induced angiogenesis via a reduction of pro-angiogenic factors in tumors. These results collectively indicate that ASF might be useful in the management of metastatic malignant tumors.</P>
Kim, Aeyung,Lim, Jong-Seok Research Institute of Women's Health Sookmyung Wom 2007 WOMEN And HEALTH Vol.3 No.2
Selenium, an essential trace element for animal and human, has been proven to maintain good health and shown to prevent several diseases. The effects of selenium compounds on tumor cell proliferation and onset of cancer are dependent on the dose and chemical composition. Current experimental evidence indicates that methylselenol (CH₃SeH), a selenium metabolite, is responsible for the dietary chemoprevention of cancers. Studies have shown that interactions between cancer cells and the extracellular matrix (ECM) are critical for the survival and invasion of metastatic cancer cells including melanoma. Despite considerable public interest in the beneficial effects of selenium compounds for melanoma chemoprevention, limited information is currently available on the molecular targets or signaling mechanisms underlying the anti-cancer effects. In this review, we introduce the anti-cancer mechanism by methylselenol based on our recent experimental data. In our studies, it was shown that methylselenol generated from selenomethionine (SeMet) plus methioninase (METase) exerts an anti-cancer effect on B16F10 melanoma cells by modulating integrin expression, altering adhesion capacity, and inducing caspase-mediated apoptosis. Furthermore, activation of p38, PKC-δ, and NF-κB was a prerequisite fur the down-regulation of integrin expression, followed by detachment-mediated apoptosis. In addition to the induction of apoptosis by the supra-nutritional level of methylselenol, non-toxic low level of methylselenol inhibited the invasive potential of B16F10 melanoma cells, particularly in association with the modulation of integrin expression. From these results, it is suggested that decreased integrin expression by methylselenol is associated with the induction of apoptosis and the inhibition of metastasis of melanoma in mice.
Kim, Aeyung,Ma, Jin Yeul Medknow PublicationsMedia Pvt Ltd 2014 Pharmacognosy magazine Vol.10 No.39
<P><B>Background:</B></P><P>Recently, our research group developed MA128, a novel herbal medicine, and demonstrated that MA128 is effective for the treatment of asthma and atopic dermatitis (AD). In particular, postinflammatory hyper-pigmentation in AD mice was improved with MA128 treatment. Thus, in this study, we determined the effect of MA128 on melanogenesis and its underlying mechanism in murine B16F10 melanoma cells.</P><P><B>Materials and Methods:</B></P><P>After treatment with MA128 at 100 and 250 μg/mL and/or alpha-melanocyte stimulating hormone (α-MSH) (1 μM), cellular melanin content and tyrosinase activity in B16F10 cells were measured. Using western blotting, expression levels of tyrosinase, tyrosinase-related protein-1 (TRP-1), TRP-2, microphthalmia-associated transcription factor (MITF), and activation of c-AMP-dependent protein kinase (PKA), c-AMP-related element binding protein (CREB) and mitogen-activated protein kinases (MAPKs) were examined.</P><P><B>Results:</B></P><P>MA128 significantly inhibited melanin synthesis and tyrosinase activity in a resting state as well as α-MSH-stimulating condition, and significantly decreased the expression of tyrosinase, TRP-1, TRP-2 and MITF. In addition, phosphorylation of PKA and CREB by α-MSH stimulation was efficiently blocked by MA128 pretreatment. Moreover, MA128 as an herbal mixture showed synergistic anti-melanogenic effects compared with each single constituent herb.</P><P><B>Conclusion:</B></P><P>MA128 showed anti-melanogenic activity through inhibition of tyrosinase activity mediated by p38 MAPK and PKA signaling pathways in B16F10 cells. These results suggest that MA128 may be useful as an herbal medicine for controlling hyper-pigmentation and as a skin-whitening agent.</P>
Kim, Aeyung,Kim, Kwang Dong,Choi, Seung-Chul,Jeong, Moon-Jin,Lee, Hee Gu,Choe, Yong-Kyung,Paik, Sang-Gi,Lim, Jong-Seok The Korean Association of Immunobiologists 2003 Immune Network Vol.3 No.3
Background: Immunization of dendritic cells (DCs) pulsed with tumor antigen can activate tumor-specific cytotoxic T lymphocytes (CTL) that are responsible for protection and regression. In this study, we examined whether the uptake of necrotic tumor cells could modulate DC phenotypes and whether the immunization of necrotic tumor cell-loaded DCs could elicit efficient tumor specific immune responses followed by a regression of established tumor burdens. Methods: We prepared necrotic tumor cell-pulsed DCs for the therapeutic vaccination and investigated their phenotypic characteristics, the immune responses induced by these DCs, and therapeutic vaccine efficacy against colon carcinoma in vivo. Several parameters including phagocytosis of tumor cells, surface antigen expression, chemokine receptor expression, IL-12 production, and NK as well as CTL activation were assessed to characterize the immune response. Results: DCs derived from mouse bone marrow efficiently phagocytosed necrotic tumor cells and after the uptake, they produced remarkably increased levels of IL-12. A decreased CCR1 and increased CCR7 expression on DCs was also observed after the tumor uptake, suggesting that antigen uptake could induce DC maturation. Furthermore, co-culturing of DCs with NK cells in vitro enhanced IL-12 production in DCs and IFN-${\gamma}$ production in NK cells, which was significantly dependent on IL-12 production and cell-to-cell contact. Immunization of necrotic tumor cell-loaded DCs induced cytotoxic T lymphocytes as well as NK activation, and protected mice against subsequent tumor challenge. In addition, intratumoral or contra-lateral immunization of these DCs not only inhibited the growth of established tumors, but also eradicated tumors in more than 60% of tumor-bearing mice. Conclusion: Our data indicate that production of IL-12, chemokine receptor expression and NK as well as CTL activation may serve as major parameters in assessing the effect of tumor cell-pulsed DC vaccine. Therefore, DCs loaded with necrotic tumor cells offer a rational strategy to treat tumors and eventually lead to prolonged survival.
KIM, AEYUNG,IM, MINJU,YIM, NAM-HIU,HWANG, YOUN-HWAN,YANG, HYE JIN,MA, JIN YEUL Spandidos Publications 2015 ONCOLOGY REPORTS Vol.34 No.2
<P>MA128, a novel herbal medicine, was previously identified and its effectiveness in the treatment of asthma and atopic dermatitis (AD) was demonstrated. In particular, post-inflammatory hyperpigmentation (PIH) in AD mice was improved by treatment with MA128. In addition, MA128 exhibited anti-melanogenic activity by inhibiting tyrosinase activity via the p38 MAPK and protein kinase A signaling pathways in B16F10 cells. In the present study, we examined whether oral administration of MA128 suppressed the in vivo tumor growth of HT1080 cells in athymic nude mice. The results showed that the daily oral administration of 75 and 150 mg/kg MA128 suppressed the tumorigenic growth of HT1080 cells efficiently. Since metastasis is a major cause of cancer-associated mortality and the greatest challenge during cancer treatment, we investigated the effect of non-toxic concentrations of MA128 on the metastatic potential of HT1080 cells. MA128 inhibited anchorage-independent colony formation, migration and invasion. Matrix metalloproteinase-9 (MMP-9) activity under resting and PMA-stimulated conditions was decreased in a dose-dependent manner by MA128 in HT1080 cells. In addition, the daily oral administration of MA128 at doses of 75 and 150 mg/kg efficiently blocked the lung metastasis of B16F10 cells that had been injected into the tail veins of C57BL/6 mice. In particular, none of the mice treated with MA128 exhibited systemic toxicity, such as body weight loss or liver and kidney dysfunction. MA128 also inhibited tumor-induced angiogenesis. Taken together, the results suggest that MA128 is a potential therapeutic agent and a safe herbal medicine for controlling malignant and metastatic cancer.</P>