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      • Induction of Apoptosis in Human Leukemic Cell Lines by Diallyl Disulfide via Modulation of EGFR/ERK/PKM2 Signaling Pathways

        Luo, Nian,Zhao, Lv-Cui,Shi, Qing-Qiang,Feng, Zi-Qiang,Chen, Di-Long,Li, Jing Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.8

        Background: Diallyl disulfide (DADS) may exert potent anticancer action both in vitro and in vivo. Although its effects on cancer are significant, the underlying mechanisms remain unknown. In this study, we sought to elucidate possible links between DADS and pyruvate kinase (PKM2). Materials and Methods: $KG1{\alpha}$, a leukemia cell line highly expressing PKM2 was used with a cell counting kit (CCK)-8 and flow cytometry (FCM) to investigate the effects of DADS. Relationships between PKM2 and DADS associated with phosphorylation of EGFR, ERK1/2 and MEK, were assessed by western blot analysis. Results: In $KG1{\alpha}$ cells highly expressing PKM2, we found that DADS could affect proliferation, apoptosis and EGFR/ERK/PKM2 signaling pathways, abrogating EGF-induced nuclear accumulation of PKM2. Conclusions: These results suggested that DADS suppressed the proliferation of $KG1{\alpha}$ cells, providing evidence that its proapoptotic effects are mediated through the inhibition of EGFR/ERK/PKM2 signaling pathways.

      • Identification of ANXA1 as a Lymphatic Metastasis and Poor Prognostic Factor in Pancreatic Ductal Adenocarcinoma

        Liu, Qing-Hua,Shi, Mei-Lin,Bai, Jin,Zheng, Jun-Nian Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.7

        Objective: The aim of this study was to investigate the clinical significance of annexin a1 (ANXA1) and provide molecular evidence to support that decreased ANXA1 expression could enhance cancer migration and invasion in pancreatic ductal adenocarcinoma (PDAC). Materials and Methods: Immunohistochemistry of a tissue microarray with 162 surgically resected PDAC specimens was performed to examine the expression of ANXA1. We also investigated the relationship between ANXA1 expression and clinicopathological factors and prognosis of PDAC patients. We further studied the role of ANXA1 in PDAC cell proliferation, migration and invasion by cell proliferation assay, migration assay and matrigel invasion assay with reduced ANXA1 expression by RNAi. Western blotting was used to detect matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) expression. We also detected MMP-9 enzyme activity by gelatin zymography. Results: Decreased expression of ANXA1 was significantly associated with poor differentiation, lymph node metastasis and advanced TNM stage of PDAC patients (p<0.05). Moreover, decreased expression of ANXA1 was correlated with poor survival (p<0.05). Furthermore, we found that ANXA1 knockdown inhibited cell proliferation, induced G1 phase cell cycle arrest, increased PDAC cell migration and invasion capacity compared with controls. In addition, Western blotting showed that ANXA1 knockdown increased the MMP-9 protein level and decreased TIMP-1 expression. Gelatin zymography showed that MMP-9 enzyme activity was also elevated. Conclusions: Negative ANXA1 expression is a most unfavorable prognostic factor for PDAC patients. ANXA1 knockdown inhibits cell proliferation by inducing G1 phase cell cycle arrest and increases migration and invasion of PDAC cells through up-regulating MMP-9 expression and activity, implying that ANXA1 may serve as a promising prognostic biomarker and therapeutic target for PDAC.

      • Antitumor Activity of Chloroquine in Combination with Cisplatin in Human Gastric Cancer Xenografts

        Zhang, Hui-Qing,Fang, Nian,Liu, Xiao-Mei,Xiong, Shu-Ping,Liao, Yu-Qian,Jin, Wen-Jian,Song, Rong-Feng,Wan, Yi-Ye Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.9

        Purpose: To investigate the antitumor activity and mechanism of chloroquine (CQ) in combination with cisplatin (DDP) in nude mice xenografted with gastric cancer SGC7901 cells. Materials and Methods: 35 cases of gastric cancer patients with malignant ascites were enrolled and intraperitoneal cisplatin injection was performed. Ascites were collected before and 5 days after perfusion for assessment of autophagy levels in cancer cells. In addition, 24 tumor-bearing mice were randomly divided into control, DDP, CQ and CQ + DDP groups. Results: In 54.3% (19/35) of patients the treatment was therapeutically effective (OR), 5 days after peritoneal chemotherapy, 13 patients had the decreased ascites Beclin-1 mRNA levels. In 16 patients who had NR, only 2 cases had decreased Beclin-1 (P=0.001). Compared with the control group, the xenograft growth in nude mice in the DDP group was low, and the inhibition rate was 47.6%. In combination with chloroquine, the inhibition rate increased to 84.7% (P<0.01). The LC3-II/I ratio, and Beclin1 and MDR1/P-gp expression were decreased, while caspase 3 protein levels increased (P<0.05). Conclusions: Antitumor ability of cisplatin was associated with autophagy activity and chloroquine can enhance chemosensitivity to cisplatin in gastric cancer xenografts nude mice.

      • Autophagy Inhibition Sensitizes Cisplatin Cytotoxicity in Human Gastric Cancer Cell Line Sgc7901

        Zhang, Hui-Qing,He, Bo,Fang, Nian,Lu, Shan,Liao, Yu-Qian,Wan, Yi-Ye Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.8

        We aimed to investigate the mechanism and effects of autophagy on cisplatin (DDP)-induced apoptosis in human gastric cancer cell line SGC7901. After SGC7901 cells were treated with DDP and/or chloroquine, cell proliferation was measured using MTT assay; cell apoptosis was determined by flow cytometry; autophagy and apotosis-related proteins expression were detected by Western blot; and quantitative analysis of autophagy after monodansylcadaverine (MDC) staining was performed using fluorescence microscopy. We found after treatment with 5 mg/L DDP for 24 h, the rates of cell apoptosis were ($21.07{\pm}2.12$)%. Autophagy, characterized by an increase in the number of autophagic vesicles and the level of LC3-II protein was observed in cells treated with DDP. After inhibition of autophagy by chloroquine, the rates of cell apoptosis were increased to ($30.16{\pm}3.54$)%, and the level of Caspase-3 and P53 protein were increased, and Bcl-2 protein was decreased. Therefore, autophagy protects human gastric cancer cell line SGC7901 against DDP-induced apoptosis, inhibition of autophagy can promote apoptosis, and combination therapy with DDP and chloroquine may be a promising therapeutic strategy for gastric cancer.

      • SCIESCOPUSKCI등재

        H<SUB>∞</SUB> Filtering for Descriptor Systems

        Yue-Peng Chen,Zu-De Zhou,Chun-Nian Zeng,Qing-Ling Zhang 대한전기학회 2006 International Journal of Control, Automation, and Vol.4 No.6

        The paper is concerned with H∞ filtering for descriptor systems. A necessary and sufficient condition is established in terms of linear matrix inequalities (LMIs) for the existence of normal filters such that the error systems are admissible and the transfer function from the disturbance to the filtering error output satisfies a prescribed H∞-norm bound constraint. When these LMIs are feasible, an explicit parameterization expression of all desired normal filter is given. All these results are yielded without decomposing the original descriptor systems, which makes the filter design procedure simple and direct. Finally, a numerical example is derived to demonstrate the applicability of the proposed approach.

      • KCI등재

        IL-33 promotes IL-10 production in macrophages: a role for IL-33 in macrophage foam cell formation

        Hai-Feng Zhang,Mao-Xiong Wu,Yong-Qing Lin,Shuang-Lun Xie,Tu-Cheng Huang,Pin-Ming Liu,Ru-Qiong Nie,Qin-Qi Meng,Nian-Sang Luo,Yang-Xin Chen,Jing-Feng Wang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

        We evaluated the role of IL-10- in IL-33-mediated cholesterol reduction in macrophage-derived foam cells (MFCs) and the mechanism by which IL-33 upregulates IL-10. Serum IL-33 and IL-10 levels in coronary artery disease patients were measured. The effects of IL-33 on intra-MFC cholesterol level, IL-10, ABCA1 and CD36 expression, ERK 1/2, Sp1, STAT3 and STAT4 activation, and IL-10 promoter activity were determined. Core sequences were identified using bioinformatic analysis and sitespecific mutagenesis. The serum IL-33 levels positively correlated with those of IL-10. IL-33 decreased cellular cholesterol level and upregulated IL-10 and ABCA1 but had no effect on CD36 expression. siRNA-IL-10 partially abolished cellular cholesterol reduction and ABCA1 elevation by IL-33 but did not reverse the decreased CD36 levels. IL-33 increased IL-10 mRNA production but had little effect on its stability. IL-33 induced ERK 1/2 phosphorylation and increased the luciferase expression driven by the IL-10 promoter, with the highest extent within the − 2000 to − 1752 bp segment of the 5′-flank of the transcription start site; these effects were counteracted by U0126. IL-33 activated Sp1, STAT3 and STAT4, but only the STAT3 binding site was predicted in the above segment. Site-directed mutagenesis of the predicted STAT3-binding sites (CTGCTTCCTGGCAGCAGAA→CTGCCTGGCAGCAGAA) reduced luciferase activity, and a STAT3 inhibitor blocked the regulatory effects of IL-33 on IL-10 expression. Chromatin immunoprecipitation (CHIP) confirmed the STAT3-binding sequences within the − 1997 to − 1700 and − 1091 to − 811 bp locus regions. IL-33 increased IL-10 expression in MFCs via activating ERK 1/2 and STAT3, which subsequently promoted IL-10 transcription and thus contributed to the beneficial effects of IL-33 on MFCs.

      • SCIESCOPUSKCI등재

        A Novel Non-phosgene Approach to the Synthesis of Methyl N-phenyl Carbamate by a Reaction of Methanol with Phenylurea

        Wang, Xin-kui,Yan, Shi-run,Li, Zhen-hua,Fan, Kang-nian,Kang, Mao-qing,Peng, Shao-yi 한국화학공학회 2004 Korean Journal of Chemical Engineering Vol.21 No.2

        A novel non-phosgene process for the synthesis of methyl N-phenyl carbamate (MPC) by a reaction of phenylurea with methanol was studied. The reaction between phenylurea and methanol was found to be a spontaneous reaction that took place in the absence of catalyst and gave MPC as the main product. Addition of a catalyst markedly influenced the reaction behavior. A basic catalyst greatly enhanced the yield of MPC, whereas an acidic catalyst promoted the formation of aniline and methyl carbamate. Moderate strength of basicity showed the best catalytic performance in the cases studied. The mechanism of reaction and catalyst functioning was discussed.

      • KCI등재

        A Novel Non-phosgene Approach to the Synthesis of Methyl N-phenyl Carbamate by a Reaction of Methanol with Phenylurea

        Shi-run Yan,Xin-kui Wang,Zhen-hua Li,Kang-nian Fan,Mao-qing Kang,Shao-yi Peng 한국화학공학회 2004 Korean Journal of Chemical Engineering Vol.21 No.2

        A novel non-phosgene process for the synthesis of methyl N-phenyl carbamate (MPC) by a reaction of phenylurea with methanol was studied. The reaction between phenylurea and methanol was found to be a spontaneous reaction that took place in the absence of catalyst and gave MPC as the main product. Addition of a catalyst markedly influenced the reaction behavior. A basic catalyst greatly enhanced the yield of MPC, whereas an acidic catalyst promoted the formation of aniline and methyl carbamate. Moderate strength of basicity showed the best catalytic performance in the cases studied. The mechanism of reaction and catalyst functioning was discussed.

      • KCI등재

        Assessment of clinical competency among TCM medical students using standardized patients of traditional Chinese medicine: A 5-year prospective randomized study

        Zeng Jinhao,Liang Shuang,Zhang Xiaotong,Yan Ran,Chen Chongli,Wen Lijuan,Xia Ting,Li Wenyuan,Lu Bingqing,Nian Qing,Yang Han,Guo Jing 한국한의학연구원 2022 Integrative Medicine Research Vol.11 No.2

        Background: Some Western medicine schools in China established standardized patient (SP) programs for medical education. However, SP programs are rarely applied to the education of traditional Chinese medicine (TCM). In this study, we evaluated the effectiveness of using standardized patient traditional Chinese medicine (SP-TCM) to improve clinical competency among TCM medical students. Methods: This study was a prospective, 2-group, parallel-training randomized trial over the course of 5 years. Data were collected from September 2016 to December 2020. Participants in each year were randomly allocated into the traditional-method training group or the SP-TCM training group (1:1) for a 3-month curriculum. Measurement of clinical competency among all trainees was based on a standardized examination composed of scores of medical record documentation, scores of TCM syndrome differentiation and therapeutic regimen, and checklist assessment from both SP-TCMs and TCM professionals. Feedback was collected using semi-constructive questionnaires from both groups. Results: Compared with those assigned to traditional-method training, those assigned to SP-TCM training demonstrated significantly greater post-training improvement in medical record documentation and TCM syndrome differentiation and therapeutic regimen. Moreover, SP-TCM trainees outscored those assigned to traditional training in the assessment for encounter performance given by independent SP-TCMs and TCM professionals. The SP-TCM method gained higher satisfaction of training efficacy and test performance than the traditional method. Conclusion: This SP-TCM program demonstrated great benefits for improving clinical competency among TCM medical students.

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