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Jingcui Yu,Songbin Fu,Peng Liu,Xiaobo Cui,Yu Sui,Guohua Ji,Rongwei Guan,Donglin Sun,Wei Ji,Fangli Liu,An Liu,Yuzhen Zhao,Yang Yu,Yan Jin,Jing Bai,Jingshu Geng,Yingwei Xue,Jiping Qi,Ki-Young Lee 한국분자세포생물학회 2011 Molecules and cells Vol.32 No.1
Previously, we identified 3 overlapping regions showing loss of heterozygosity (LOH, R_1-R_3 from 11 to 30 cM) on chromosome 17 in 45 primary gastric cancers (GCs). The data indicated the presence of tumor suppressor genes (TSGs) on chromosome 17 involved in GC. Among the putative TSGs in these regions, HIC1 (in SR_1) and TOB1 (in SR_3) remain to be examined in GC. By immunohistochemistry (IHC), methylation-specific PCR (MSP) and western blot, we evaluated the expression and regulation status for HIC1 and TOB1 protein in GC. We narrowed down the deletion intervals on chromosome 17 and defined five smaller LOH subregions, SR_1-SR_5 (0.54 to 3.42 cM), in GC. We found that HIC1 had downregulated expression in 86% (91/106) and was methylated in 87% (26/30) of primary GCs. Of the primary GCs showing downregulation of HIC1 protein, 75% (18/24) had methylated HIC1 gene. TOB1 was either absent or expressed at reduced levels in 75% (73/97) of the GC samples. In addition, a general reduction was found in total and the ratio of unphosphorylated to phosphorylated TOB1 protein levels in the differentiated GC cell lines. Further analysis revealed significant simultaneous downregulation of both HIC1 and TOB1 protein in GC tissue microarray samples (67%, 52/78) and in primary GCs (65%, 11/17). These results indicate that silencing of HIC1 and TOB1 expression is a common occurrence in GC and may contribute to the development and progression of the disease.
Liu, HongLing,Wu, JunHua,Min, Ji Hyun,Hou, Peng,Song, Ah-Young,Kim, Young Keun IOP Pub 2011 Nanotechnology Vol.22 No.5
<P>The Fe<SUB>3</SUB>O<SUB>4</SUB>–Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> core–shell nanoparticles were prepared by one-pot non-aqueous nanoemulsion with the assistance of a biocompatible triblock copolymer, poly(ethylene glycol)-<I>block</I>-poly(propylene glycol)-<I>block</I>-poly(ethylene glycol) (PEO–PPO–PEO), integrating the magnetic properties of Fe<SUB>3</SUB>O<SUB>4</SUB> and the bioactive functions of Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> into single entities. The Fe<SUB>3</SUB>O<SUB>4</SUB> nanoparticles were pre-formed first by thermal reduction of Fe(acac)<SUB>3</SUB> and then the Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> layer was coated by simultaneous deposition of Ca<SUP>2 + </SUP> and PO<SUB>4</SUB><SUP>3 − </SUP>. The characterization shows that the combination of the two materials into a core–shell nanostructure retains the magnetic properties and the Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> shell forms an hcp phase (<I>a</I> = 7.490 Å, <I>c</I> = 9.534 Å) on the Fe<SUB>3</SUB>O<SUB>4</SUB> surface. The magnetic hysteresis curves of the nanoparticles were further elucidated by the Langevin equation, giving an estimation of the effective magnetic dimension of the nanoparticles and reflecting the enhanced susceptibility response as a result of the surface covering. Fourier transform infrared (FTIR) analysis provides the characteristic vibrations of Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> and the presence of the polymer surfactant on the nanoparticle surface. Moreover, the nanoparticles could be directly transferred to water and the aqueous dispersion–collection process of the nanoparticles was demonstrated for application readiness of such core–shell nanostructures in an aqueous medium. Thus, the construction of Fe<SUB>3</SUB>O<SUB>4</SUB> and Ca<SUB>3</SUB>(PO<SUB>4</SUB>)<SUB>2</SUB> in the core–shell nanostructure has conspicuously led to enhanced performance and multi-functionalities, offering various possible applications of the nanoparticles.</P>
( Peng Cheng Liu ),( Ji Young Lim ),( Hee Seo Kim ),( Jong Hwa Kim ),( Keon Sang Chae ) 한국균학회 2012 Mycobiology Vol.40 No.3
The amino acid sequence of the mheA gene of Aspergillus oryzae encodes a putative metallothionein-like protein 1. The size of the mheA transcript was 497 nt and the mheA promoter was induced by glucose, consistent with results of analysis by Northern hybridization and with the pdcA promoter, respectively.
Zhao, Ji-An,Peng, Li,Geng, Cui-Zhi,Liu, Yue-Ping,Wang, Xu,Yang, Hui-Chai,Wang, Shi-Jie Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.5
The purpose of the present study was to evaluate the preventive effects of hydrazinocurcumin (HZC) on diethylnitrosamine (DEN)-induced hepatocarcinogenesis in a male Sprague Dawley (SD) rat model. One hundred and twenty male SD rats used in this study were divided into six groups. Those receiving DEN with curcumin (CUR) or HZC were studied compared with the DEN-alone group. The study demonstrated that DEN induced severe histological and immunohistochemical changes in liver tissues, significantly increasing the levels of liver marker enzymes (alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), ${\gamma}$-glutamyltransferase (GGT) and total bilirubin level (TBL)). The hepatocarcinoma incidences were 100.0%, 36.7% and 20.0% in the DEN-alone, DEN-CUR and DEN-HZC groups, respectively. Although macroscopic and microscopic features suggested that both CUR and HZC were effective in inhibiting DEN-induced hepatocarcinogenesis, HZC was exerted a stronger influence. Immunohistochemical analysis with PCNA demonstrated significantly differences among the groups (all P < 0.05). Taken together, the results suggested application of CUR and HZC could prevent the occurrence of carcinogenesis and HZC may be a more potent compound for prevention of DEN-induced hepatocarcinogenesis in rats than CUR.
Three New 11,20-Epoxy-ent-kauranoids from Isodon rubescens
Xu Liu,Ji Zhou Wu,Rui Zhan,Wei Guang Wang,Xue Du,Yan Li,Peng Zhang,Jian Xin Pu,Han Dong Sun 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.12
Three rare and new 11,20-epoxy-ent-kaurane diterpenoids, named jianshirubesins D-F (1-3), along with one known analogue (4), were isolated from the aerial parts of Isodon rubescens. Their structures were established by analysis of spectroscopic data. Found in the MTT assay to evaluate the cytotoxicity of compounds 1, 2, and 4, only 1 could selectively inhibit certain cell lines from proliferating. In addition, a simple structure-activity relationship discussion might suggest a new bioactive moiety, different from the α,β-unsaturated ketone group.
Zhifeng Liu,Jingjing Ji,Dong Zheng,Lei Su,Tianqing Peng,Jing Tang 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-
To explore the role of calpain and its signaling pathway in lipopolysaccharide (LPS)-induced acute kidney injury (AKI), animal models of endotoxemia were established by administration of LPS to mice with endothelial-specific Capn4 knockout (TEK/Capn4−/−), mice with calpastatin (an endogenous calpain inhibitor) overexpression (TgCAST) and mice with myeloid-specific Capn4 knockout (LYZ/Capn4−/−). Mouse pulmonary microvascular endothelial cells (PMECs) were used as a model of the microvascular endothelium and were stimulated with LPS. Renal function, renal inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) expression, cellular apoptosis, plasma and renal levels of NO and reactive oxygen species (ROS), and phosphorylation of mitogenactivated protein kinase (MAPK) family members (p38, ERK1/2, and JNK1/2) were examined. Moreover, a calpain inhibitor, calpastatin overexpression adenoviruses and MAPK inhibitors were used. Significant renal dysfunction was induced by LPS stimulation, and recovery was observed in TEK/Capn4−/− and Tg-CAST mice but not in LYZ/ Capn4−/− mice. Endothelial Capn4 knockout also abrogated the LPS-induced increases in renal iNOS expression, caspase-3 activity and apoptosis and plasma and renal NO and ROS levels but did not obviously affect renal eNOS expression. Moreover, LPS increased both calpain and caspase-3 activity, and only the expression of iNOS in PMECs was accompanied by increased phosphorylation of p38 and JNK. Inhibiting calpain activity or p38 phosphorylation alleviated the increased iNOS expression, NO/ROS production, and cellular apoptosis induced by LPS. These results suggest that endothelial calpain plays a protective role in LPS-induced AKI by inhibiting p38 phosphorylation, thus attenuating iNOS expression and further decreasing NO and ROS overproduction-induced endothelial apoptosis.