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Ho, Manh Tin,Kim, Young Mee,Yu, Dae-Yeul,Lee, Dae Ho,Cho, Moonjae,Hyun, Changlim The Korean Society for Applied Biological Chemistr 2014 Applied Biological Chemistry (Appl Biol Chem) Vol.57 No.4
Hepatic stellate cells (HSCs) are the main extra cellular matrix-producing cells in the liver. Several reports have indicated that activated HSCs are involved in hepatic carcinogenesis by way of transforming growth factor ${\beta}$ (TGF-${\beta}$) secretion. This study aimed to investigate the effects of TGF-${\beta}$, derived from HSCs activated by the chronic hepatitis B virus x protein (HBx), on the transdifferentiation of hepatocytes into hepatocarcinoma cells. Normal hepatocytes (the Chang liver cell line) were treated with a low concentration of TGF-${\beta}$ for 2 weeks, after which cell cycle- and cell signaling-related protein expression was analyzed. Long-term treatment of TGF-${\beta}$ clearly induced the proliferation and the expression of cancer signaling proteins in the Chang cell line. TGF-${\beta}$ treatment also increased the expression of c-Jun N-terminal kinase (JNK) and c-Myc, indicating that induction of the JNK/pSmad3/c-Myc oncogenic signaling pathway is involved in hepatocyte transformation. Similar results were observed after culturing Chang cells with conditioned media derived from the activated LX-2 hepatic stellate cell line, suggesting that TGF-${\beta}$ paracrine effects are involved in the transformation of hepatocyte cells into hepatocarcinoma cells. Immunohistochemical results showed that the livers from HBx transgenic mice were composed of more activated HSCs and produced more TGF-${\beta}$ compared with those from normal mice. The TGF-${\beta}$ secreted from HBx-infected HSCs might induce transdifferentiation of hepatocytes into hepatocarcinoma, which is the fact that suggested a potential knowledge on liver cancer inhibition.
Manh Tin Ho,이대호,현창림,유대열,조문재,김영미 한국응용생명화학회 2014 Applied Biological Chemistry (Appl Biol Chem) Vol.57 No.4
Hepatic stellate cells (HSCs) are the main extra cellularmatrix-producing cells in the liver. Several reports have indicatedthat activated HSCs are involved in hepatic carcinogenesis by wayof transforming growth factor β (TGF-β) secretion. This studyaimed to investigate the effects of TGF-β, derived from HSCsactivated by the chronic hepatitis B virus x protein (HBx), on thetransdifferentiation of hepatocytes into hepatocarcinoma cells. Normal hepatocytes (the Chang liver cell line) were treated witha low concentration of TGF-β for 2 weeks, after which cell cycleandcell signaling- related protein expression was analyzed. Longtermtreatment of TGF-β clearly induced the proliferation and theexpression of cancer signaling proteins in the Chang cell line. TGF-β treatment also increased the expression of c-Jun Nterminalkinase (JNK) and c-Myc, indicating that induction of theJNK/pSmad3/c-Myc oncogenic signaling pathway is involved inhepatocyte transformation. Similar results were observed afterculturing Chang cells with conditioned media derived from theactivated LX-2 hepatic stellate cell line, suggesting that TGF-βparacrine effects are involved in the transformation of hepatocytecells into hepatocarcinoma cells. Immunohistochemical resultsshowed that the livers from HBx transgenic mice were composedof more activated HSCs and produced more TGF-β comparedwith those from normal mice. The TGF-β secreted from HBxinfectedHSCs might induce transdifferentiation of hepatocytesinto hepatocarcinoma, which is the fact that suggested a potentialknowledge on liver cancer inhibition.
Ho, Manh Tin,Kang, Hyun Sik,Huh, Jung Sik,Kim, Young Mee,Lim, Yoongho,Cho, Moonjae MDPI 2014 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.15 No.7
<P>Wound healing plays an important role in protecting the human body from external infection. Cell migration and proliferation of keratinocytes and dermal fibroblasts are essential for proper wound healing. Recently, several studies have demonstrated that secondary compounds produced in plants could affect skin cells migration and proliferation. In this study, we identified a novel compound DK223 ([1<I>E</I>,2<I>E</I>-1,2-bis(6-methoxy-2<I>H</I>-chromen-3-yl)methylene]hydrazine) that concomitantly induced human keratinocyte migration and dermal fibroblast proliferation. We evaluated the regulation of epithelial and mesenchymal protein markers, such as E-cadherin and Vimentin, in human keratinocytes, as well as extracellular matrix (ECM) secretion and metalloproteinase families in dermal fibroblasts. DK223 upregulated keratinocyte migration and significantly increased the epithelial marker E-cadherin in a time-dependent manner. We also found that reactive oxygen species (ROS) increased significantly in keratinocytes after 2 h of DK223 exposure, returning to normal levels after 24 h, which indicated that DK223 had an early shock effect on ROS production. DK223 also stimulated fibroblast proliferation, and induced significant secretion of ECM proteins, such as collagen I, III, and fibronectin. In dermal fibroblasts, DK223 treatment induced TGF-β1, which is involved in a signaling pathway that mediates proliferation. In conclusion, DK223 simultaneously induced both keratinocyte migration via ROS production and fibroblast proliferation via TGF-β1 induction.</P>
Ho, Manh Tin,Koh, Dongsoo,Cho, Moonjae 한국응용생명화학회 2014 Applied Biological Chemistry (Appl Biol Chem) Vol.57 No.6
Ultraviolet (UV) radiation in sunlight can induce skin ageing and photo-carcinogenesis. UV may also induce melanin production and wrinkle formation. Recently, natural secondary compounds have been reported to have protective effects against UV light. In this study, the effects of two different compounds, glycitin and 3-(2,4,6-trimethoxyphenyl)-2,3-dihydro-1H-benzo[f] chromen-1-one (TDB), on human dermal fibroblasts and melanocytes were investigated. At first, only TDB was used on melanocyte cells to test whether it inhibited the proliferation of these cells. Then, a mixture of glycitin and TDB was tested on human dermal fibroblasts for 48 h in order to investigate its effect on proliferation, collagen production, and metalloproteinase family expression. The TDB treatment alone not only inhibited the proliferation of melanocytes but also increased extra cellular matrix production in dermal fibroblasts and cell viability. The mixture of glycitin and TDB markedly increased fibroblast proliferation and helped to maintain fibroblast viability in the face of UV-induced and $H_2O_2$-induced damages. This co-treatment also significantly promoted collagen IV expression and accelerated total collagen secretion. In addition, the metalloproteinase (MMPs) family such as MMP1, MMP2, and MMP7 were down-regulated at the transcriptional level. In conclusion, the mixture of glycitin and TDB induced fibroblast proliferation even when these fibroblasts were damaged by UV exposure and $H_2O_2$, whereas augmented collagen production and the inhibition of MMPs reduced wrinkle formation and decreased melanocyte proliferation, suggesting a potential use in UV-protective therapy.
Manh Tin Ho,고동수,조문재 한국응용생명화학회 2014 Applied Biological Chemistry (Appl Biol Chem) Vol.57 No.6
Ultraviolet (UV) radiation in sunlight can induce skinageing and photo-carcinogenesis. UV may also induce melaninproduction and wrinkle formation. Recently, natural secondarycompounds have been reported to have protective effects againstUV light. In this study, the effects of two different compounds,glycitin and 3-(2,4,6-trimethoxyphenyl)-2,3-dihydro-1H-benzo[f]chromen-1-one (TDB), on human dermal fibroblasts andmelanocytes were investigated. At first, only TDB was used onmelanocyte cells to test whether it inhibited the proliferation ofthese cells. Then, a mixture of glycitin and TDB was tested onhuman dermal fibroblasts for 48 h in order to investigate its effecton proliferation, collagen production, and metalloproteinase familyexpression. The TDB treatment alone not only inhibited theproliferation of melanocytes but also increased extra cellularmatrix production in dermal fibroblasts and cell viability. Themixture of glycitin and TDB markedly increased fibroblastproliferation and helped to maintain fibroblast viability in the faceof UV-induced and H2O2-induced damages. This co-treatmentalso significantly promoted collagen IV expression and acceleratedtotal collagen secretion. In addition, the metalloproteinase (MMPs)family such as MMP1, MMP2, and MMP7 were down-regulatedat the transcriptional level. In conclusion, the mixture of glycitinand TDB induced fibroblast proliferation even when thesefibroblasts were damaged by UV exposure and H2O2, whereasaugmented collagen production and the inhibition of MMPsreduced wrinkle formation and decreased melanocyte proliferation,suggesting a potential use in UV-protective therapy.
Seo, Ga Young,Ho, Manh Tin,Bui, Ngoc Thuy,Kim, Young Mee,Koh, Dongsoo,Lim, Youngho,Hyun, Changlim,Cho, Moonjae BioMed Central 2015 JOURNAL OF BIOMEDICAL SCIENCE -BASEL- Vol.22 No.1
<P><B>Background</B></P><P>Wound healing is an intricate process whereby the skin repairs itself after injury. The epithelial-mesenchymal transition (EMT) is associated with wound healing and tissue regeneration. Naphthochalcone derivatives have various pharmaceutical properties. We investigated the effect of a novel naphthochalcone derivative, 2-(5-(2,4,6-trimethoxyphenyl)-4,5-dihydro-1H-pyrazol-3-yl)naphthalen-1-ol (TDPN), on dermal wound healing <I>in vivo</I> and the migration of keratinocytes <I>in vitro.</I></P><P><B>Result</B></P><P>We investigated the effect of TDPN on signaling pathway and epithelial-mesenchymal transition through protein and transcriptional expression. The TDPN treatment accelerated dermal closure about 3 days and remodeling of dermis. We found that treatment with TDPN induced the migration of keratinocytes but not cytotoxicity. TDPN induced the phosphorylation of ERK and AKT. TDPN-treated cells showed loss of adherence protein and showed induction of the transcriptional factor Slug, mesenchymal marker, and fibronectin. Moreover, TDPN treatment induced the expression of matrix metalloproteinase-1 (MMP-1), which degrades specific components of the extracellular matrix, thereby providing new substrates that facilitate migration and invasion. MMP expression is considered to be one of the major attributes acquired by cells after EMT.</P><P><B>Conclusion</B></P><P>We propose that a novel naphthochalcone derivative TDPN is capable of promoting keratinocyte migration <I>via</I> the induction of EMT resulting acceleration of wound closure and matrix remodeling.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/s12929-015-0141-3) contains supplementary material, which is available to authorized users.</P>
한상훈,Ngoc Thuy Bui,Manh Tin Ho,김영미,조문제,신동복 대한암학회 2016 Cancer Research and Treatment Vol.48 No.3
Purpose One of the features in cancer development is the migration of cancer cells to form metastatic lesions. CYR61 protein promotes migration and the epithelial-mesenchymal transition in several cancer cell types. Evidence suggests that CYR61 and dexamethasone are relevant to colorectal cancer. However, relationships between them and colorectal cancer are still unclear. Understanding the molecular mechanism of colorectal cancer progression related with CYR61 and dexamethasone, which is widely used for combination chemotherapy, is necessary for improved therapy. Materials and Methods We used colorectal cancer cells, HCT116, co-treated with transforming growth factor !1 (TGF-!1) and dexamethasone to examine the inhibitory migration effect of dexamethasone by migratory assay. Alternatively, both migratory pathways, expression of AKT and ERK, and the target factor CYR61 was also tested by co-treatment with TGF-!1 and dexamethasone. Results We report that dexamethasone significantly inhibited TGF-!1–induced cell migration, without affecting cell proliferation. Importantly, we observed that TGF-!1 promoted the epithelial- mesenchymal transition process and that dexamethasone co-treatment abolished this effect. ERK and AKT signaling pathways were found to mediate TGF-!1–induced migration, which was inhibited by dexamethasone. In addition, TGF-!1 treatment induced CYR61 expression whereas dexamethasone reduced it. These observations were compatible with the modulation of migration observed following treatment of HCT116 cells with human recombinant CYR61 and anti-CYR61 antibody. Our results also indicated that TGF-!1 enhanced collagen I and reduced matrix metalloproteinase 1 expression, which was reversed by dexamethasone treatment. Conclusion These findings suggested that dexamethasone inhibits AKT and ERK phosphorylation, leading to decreased CYR61 expression, which in turn blocks TGF-!1–induced migration.
( So Jin Bing ),( Manh Tin Ho ),( Phorl Sophors ),( Sang Gyu Park ),( Young Min Yun ),( Young Heun Jee ),( Moon Jae Cho ) 한국응용생명화학회(구 한국농화학회) 2015 Journal of Applied Biological Chemistry (J. Appl. Vol.58 No.1
Extracted mushroom water showed an ability to suppress the accumulation of body fat in female mice after feeding 5 weeks with high fat diet. Particularly, in parametrial and mesenteric adipose, it significantly reduced 44 and 47% of weight, respectively. In non-obese mice, maturated NK cell (CD11bhiCD27lo) population were increased (70.9±3.8% ) in mushroom water fed mice compared to control (61.4±4.3%) and NK cell population were augmented in mushroom fed mice compared to control.