Cancer biologyB-17-86Elevated fibroblast growth factor-inducible 14 expression levels promotethe growth of gastric cancer cell via nuclear factor-κB and correlate withpoor patient outcomeOh-Hyung Kwon¹ , ², Sung-Joon Park¹ , ³, Mirang Kim¹, Jeong-Hwan Kim¹, Seung-Moo Noh⁴, Kyu-Sang Song5, Hyang-Sook Yoo¹, Sang-Gi Paik², Yeul-Hong Kim³,Seon-Young Kim¹and Yong Sung Kim¹¹Medical Genomics Research Center, KRIBB, Daejeon 305-806, Korea, ²Department of BiologicalScience, College of Biological Sciences and Biotechnology, Chungnam National University, Daejeon305-764, Korea, ³Division of Oncology-Hematology, Department of Internal Medicine, KoreaUniversity Anam Hospital, Korea University College of Medicine, <strong>12</strong>6-1 Anam-dong 5 ga,Seongbuk-gu, Seoul 136-705, Korea, ⁴Department of General Surgery, 5 Department of Pathology,College of Medicine, Chungnam National University, Daejeon 301-747, KoreaThe fibroblast growth factor-inducible 14 (Fn14) gene encodes a type I transmembrane protein thatbelongs to the tumor necrosis factor receptor superfamily, and regulates multiple cellular processesin diverse physiological and pathological conditions, including cancer. Here, we report an importantrole for Fn14 in regulating growth of gastric cancer cells. Previous gene expression data analysishad shown that Fn14 was up-regulated in various tumor tissues, including gastric cancer. By realtimeRT-PCR, we showed that Fn14 was overexpressed in gastric tumor tissues compared withnormal tissues. Furthermore, Fn14 expression levels inversely correlated with gastric cancerpatient survival. By both ectopic overexpression and shRNA-mediated knockdown of Fn14, weshowed that the expression levels of Fn14 affected cell growth in gastric cancer. The effect of Fn14on cell growth was mediated by the NF-κB activity, and eventually by the transcriptional regulationof anti-apoptotic Bcl-2 family genes (Bcl-xL and Bcl-w). These results suggest that Fn14 may playan important role in gastric tumor growth by regulating NF-κB mediated anti-apoptosis pathway,and be one of the prognostic markers for gastric cancer patientsB-17-87Screening and characterization of TRAIL-sensitizing chemicalsMin-Jeong Jang and Seok-Hyun KimCarcinogenesis branch, Research Institute, National Cancer Center, <strong>11</strong>1 Jungbalsan-ro, Ilsandonggu,Goyang-si, Gyeonggi-do 4<strong>10</strong>-769, KoreaTRAIL is a promising cancer-specific apoptosis inducing ligand for human tumor cells.Unfortunately, TRAIL is not able to induce apoptosis in some population of cancer celllines. This might implicate that TRAIL treatment alone would be not so effective in somecancer patent. To overcome this potential limitation, we screened about 4,<strong>00</strong>0 smallmolecules from Chemdiv and tried to find the effective small molecules that can sensitizeTRAIL-resistant cancer cell lines. We successfully identified three small molecules thatsensitized TRAIL-resistant HT-29 cell line which is TRAIL-resistant. We also confirmedTRAIL-sensitizing activity of these chemicals in other TRAIL-resistant cell lines. TheTRAIL-sensitizing chemical decreased cell survival in TRAIL-resistant cell lines whichwas identified by crystal violet staining. Significant apoptosis enhancement bycombination of TRAIL with chemical was confirmed through subG1 analysis, PARP andcaspase 3 cleavage in TRAIL-resistant cell lines. Interestingly, the chemical decreasedMcl-1 expression and reduced TRAIL-mediated induction of Mcl-1. It is similar result of awell-known combination of TRAIL with sorafenib. This result led us to speculate Mcl-1might be the key molecule responsible for the TRAIL-sensitizing mechanism.B-17-89Induction of apoptosis by glycoprotein Isolated from Laminaria japonicawas associated with the down-regulation of telomerase andcyclooxygenase-2 activity in AGS human gastric cancer cellsMin Ho Han 1 , Gi Young Kim 2 , Sung-Kwon Moon 3, 5 , Wun-Jae Kim 4 , Taek-Jeong Nam 51, 5, 6and Yung Hyun Choi¹Department of Biomaterial Control and Blue-Bio Industry RIC, Dongeui University, Busan 614-714, ²Department of Marine Life Science, Jeju National University, Jeju 690-756, ³Department ofFood and Biotechnology, Chungju National University, Chungbuk 380-702, ⁴Department ofUrology, Chungbuk National University College of Medicine, Chungbuk 361-763, 5 Department ofFood Science and Biotechnology, Pukyong National University, Busan 608-737, 6 Department ofBiochemistry, Dongeui University College of Oriental Medicine, Busan 614-052, KoreaIn this study, we investigated the possible mechanisms by which glycoprotein isolated fromLaminaria japonica (LJGP) exerts its anti-cancer action in cultured AGS cells. LJGPtreatment of AGS cells resulted in inhibition of growth and induction of apoptosis. Theincrease in apoptosis was associated with up-regulation of pro-apoptotic Bax expression,down-regulation of anti-apoptotic Bcl-2 and IAP family members, and activation ofcaspase-3 and -9. LJGP treatment markedly down-regulated the activity of telomerase andexpression of human telomerase reverse transcriptase, a main determinant of telomeraseenzymatic activity, with inhibition of Sp1 and c-Myc expression in a concentrationdependentmanner. Furthermore, LJGP treatment also caused a progressive decrease inthe expression levels of COX-2 without significant changes in the levels of COX-1, whichwas correlated with a decrease in prostaglandin E2 synthesis. These results provideimportant new insights into the possible molecular mechanisms of the anti-cancer activityof LJGP. [This work was supported by the National Research Foundation of Korea and theproject funded by the Ministry of Land, Transport and Maritime Affairs, South Korea.]B-17-90Thioredoxin modulates radiation stress response and sensitivity toapoptosis induced by gamma irradiationSeol-Hee Kim, Ji-Yoon Ryu. Sinae Ahn and Choong-Eun LeeLaboratory of Immunology, Department of Biological Science, Sungkyunkwan University, Suwon440-746, KoreaThioredoxin plays a major role in the control of cellular redox status. Since gammaradiation can evoke oxidative stress conditions and activation of various intracellularsignaling pathways associated with cellular defense mechanism, we have investigatedfunction of thioredoxin as a radition stress sensor against ROS-mediated DNA damage.In various tumor cell lines which differ in p53 status, thioredoxin was induced within 3-4 hupon radiation or oxidative stress response. The overexpression of thioredoxin, however,resulted in differential effects on the stress and survival signaling pathways depending onthe cell type. In p53 wt tumor cells, thioredoxin promoted p53 activation, p21 induction,and led to the increase in apoptotic response induced by gamma irradiation. In contrast,in tumor cells with p53 mutation, thioredoxin suppressed the radiation-induced JNK, p38,but increased Erk activity, which probably contributed to anti-apoptotic function ofthioredoxin in these cells. We performed microarray analysis with gene chips to identifytarget genes responsible for the modulatory effects of thioredoxin. The results alsosuggest that thioredoxin affects various apoptosis/survival and ROS-related pathways inresponse to radiation stress in a cell type-specific manner.B-17-88Inhibition of matrix metalloproteinase activities and tightening of tightjunctions by diallyl disulfide in human gastric carcinoma AGS cellsHyun Soo Park 1 , Gi-Young Kim 2 , Nam Deuk Kim¹, Hye Jin Hwang 3, 4 , Young-WhanChoi 5 and Yung Hyun Choi 6, *¹Department of Pharmacy, Pusan National University, Busan 609-735, ²Department of MarineLife Sciences, Jeju National University, Jeju 690-756, ³Department of Food and Nutrition, and⁴Blue-Bio Industry RIC, Dongeui University, Busan 614-714, 5 Department of HorticulturalBioscience, Pusan National University, Miryang 627-706, 6 Departments of Oriental Medicine andBiomaterial Control, and, Dongeui University, Busan 614-052, KoreaThe effect of diallyl disulfide (DADS), a major component of an oil-soluble allyl sulfidegarlic (Allium sativum) derivative, on the correlation between anti-invasive activity andtightening of tight junctions (TJs) was investigated in human gastric adenocarcinomaAGS cells. Our data indicated that the inhibitory effects of DADS on cell motility andinvasiveness were found to be associated with increased tightness of the TJs, which wasdemonstrated by an increase in transepithelial electrical resistance. Activities of MMP-2and -9 in AGS cells were dose-dependently inhibited by treatment with DADS, and thiswas also correlated with a decrease in expression of their mRNA and proteins; however,TIMP-1 and -2 mRNA levels and proteins were increased. Additionally, immunoblottingresults indicated that DADS repressed the levels of claudin proteins, major componentsof TJs that play key roles in control and selectivity of paracellular transport. Althoughfurther studies are needed, these results suggest that DADS treatment may inhibit tumorcell motility and invasion and, therefore, act as a dietary source to decrease the risk ofcancer metastasis. [Supported by a grant (Code #7-19-42) from Rural DevelopmentAdministration]B-17-91Rsf-1, a protein involved in chromatin remodeling, is functionallyrelated to the activation of aurora B kinaseHo-Soo Lee, Sunyoung Chae, Hyeseong ChoDepartment of Biochemistry and Molecular Biology, Ajou University School of Medicine andDepartment of Molecular Science and Technology, Ajou University, Suwon, KoreaRsf-1/HBxAP interacts with hSNF2H, a ATPase to form a chromatin remodeling complex,RSF (remodeling and spacing factor). Recently, Rsf-1 is suggested to be related to beinvolved in centromere formation. Here, we show that Rsf-1/HBxAP protein level is highin mitosis where it localizes at the centromeres. By depletion of Rsf-1/HBxAP, we foundsevere defects in chromosomal congression, resulting in accumulation of prometaphasecells. Despite the defects in congression, analysis of time-laps images showed theacceleration of mitotic progression, indicating that the mitotic checkpoint is compromisedin Rsf-1 deficient cells. In Rsf-1 depleted cells, Aurora B and hBubR1 properly localize tocentromeres and kinetochores, respectively. However, Aurora B kinase activity wassignificantly decreased in Rsf-1/HBxAP or hSNF2H depleted cells. This study proposethe first evidence that Rsf1/HBxAP is a key component in mitosis.182 Korean Society for Biochemistry and Molecular Biology
Cancer biology
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