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PING CHEN,QING-SHENG WU,YA-PING DING,ZI-CHUN ZHU 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2011 NANO Vol.6 No.4
In this paper, the cisplatin composite micro/nanofibers were prepared by electrospinning. Average diameter of the typical products was about 700 nm, and cisplatins were incorporated in biodegradable poly (L-lactic acid) fibers. The controlled release of cisplatin can be gained for long time. The possible mechanisms of cisplatin release in the PBS and the PBS with proteinase K were discussed. 3-(4, 5)-dimethylthiahiazo-(-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) method was used to test antitumor activities in vitro against human lung tumor spc-a-1 cells. When incubation time was 24 h, the same content of cisplatin from virgin cisplatin and the composite fibers has almost equal antitumor activity in vitro. However, when incubation time was 48 h, the composite fibers show much higher antitumor activity than the virgin cisplatin. The system may be useful in the postoperative local chemotherapy and have clinical applications as an implantable drug for tumor in the future.
Guo, Yu,Liao, Ya-Ping,Zhang, Ding,Xu, Li-Sha,Li, Na,Guan, Wei-Jun,Liu, Chang-Qing Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.5
Although nucleolar protein nucleostemin (NS) is essential for cell proliferation and early embryogenesis and expression has been observed in some types of human cancer and stem cells, the molecular mechanisms involved in mediation of cell proliferation and cell cycling remains largely elusive. The aim of the present study was to evaluate NS as a potential target for gene therapy of human breast carcinoma by investigating NS gene expression and its effects on SKBR-3 cell proliferation and apoptosis. NS mRNA and protein were both found to be highly expressed in all detected cancer cell lines. The apoptotic rate of the pcDNA3.1-NS-Silencer group ($12.1-15.4{\pm}3.8%$) was significantly higher than those of pcDNA3.1-NS ($7.2-12.0{\pm}1.7%$) and non-transfection groups ($4.1-6.5{\pm}1.8%$, P<0.01). MTT assays showed the knockdown of NS expression reduced the proliferation rate of SKBR-3 cells significantly. Matrigel invasion and wound healing assays indicated that the number of invading cells was significantly decreased in the pcDNA3.1-NS-siRNA group (P<0.01), but there were no significant difference between non-transfected and over-expression groups (P>0.05). Moreover, RNAi-mediated NS down-regulation induced SKBR-3 cell G1 phase arrest, inhibited cell proliferation, and promoted p53 pathway-mediated cell apoptosis in SKBR-3 cells. NS might thus be an important regulator in the G2/M check point of cell cycle, blocking SKBR-3 cell progression through the G1/S phase. On the whole, these results suggest NS might be a tumor suppressor and important therapeutic target in human cancers.
Assembling Synthesis of Barium Chromate Nano-superstructures Using Eggshell Membrane as Template
Liu, Jin-Ku,Wu, Qing-Sheng,Ding, Ya-Ping,Yi, Yu Korean Chemical Society 2004 Bulletin of the Korean Chemical Society Vol.25 No.12
The branch-like, feather-like $BaCrO_4$ nano-superstructures were synthesized with bioactive eggshell membrane as directing and assembly template. Studies on the two products revealed that they formed through the self-assembly of nanoparticles, and that the optical properties of the products were different from $BaCrO_4$ bulk materials.
Synthesis and Optical Properties of the Semiconductor Lead Sulfide Nanobelts
Yang, Xiao hong,Wu, Qing Sheng,Ding, Ya Ping,Liu, Jin ku Korean Chemical Society 2006 Bulletin of the Korean Chemical Society Vol.27 No.3
The semiconductor PbS nanobelts (width 50-120 nm and length over 3 $\mu$m) were self-assembled in a simple reverse micelle solvent system containig the surfactant of polyoxyethylene (9) dodecy ether $(C_{12}E_9)$. The nanobelts synthesized were found to possess cube galena poly-crystal structure with high purity when analyzed by ED and X-ray diffraction. Significant “blue shift” from bulk material was observed on the PbS nanobelts using photoluminescence and UV-Vis spectroscopy. A mechanism involving the possible formation of nanobelts based on surfactant template was also proposed.
Guo, Yu,Xu, Li-Sha,Zhang, Ding,Liao, Ya-Ping,Wang, Hai-ping,Lan, Zhi-Hui,Guan, Wei-Jun,Liu, Chang-Qing Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.8
Objectives: To investigate the effects of betaine on HeLa cell growth and apoptosis and molecular mechanisms. Materials and Methods: Concentrations of 0.1, 1.0, 5.0, 20.0, 100.0 mg/ml of betaine were used to evaluate the anticancer efficacy for HeLa cells respectively, and MCF-10A was also detected as a normal diploid cell control. Results: We found that proliferation of HeLa cells was inhibited significantly upon exposure to increasing betaine levels with the MTT test (p<0.05). The percentage of S phase cells in the low dose groups (<5mg/ml) were distinctly higher than in high dose groups, and the rates of Sub-G1 phase were the opposite (p<0.01); A high concentration of betaine (>5.0mg/ml) significantly promoted the apoptosis of HeLa cells (p<0.01). SOD activities of the low dose groups were slightly higher than the control group (p<0.05) and there were obvious synchronicity and correlation among the expression of promoting apoptosis genes Bax, P53, Caspase 3 and apoptosis suppression gene Bcl-2. In response to an apoptosis-inducing stimulus, p53 and cyclin D1 could be activated with blockage of the cell cycle at G1/S or S/G2 checkpoints. Conclusions: Our data showed that betaine could promote HeLa cells proliferation in vitro at low concentrations. In contrast, high concentrations could significantly inhibit cell growth and migration, and induce apoptosis of HeLa cells through caspase 3 signaling and further promoted necrosis. This might imply that betaine exhibits tumoricidal effects and acts as a biological response modifier in cancer treatment by inducing apoptosis and cell cycle arrest in a dose and time-dependent manner.
Lu, De-Yi,Mao, Xu-Hua,Zhou, Ying-Hui,Yan, Xiao-Long,Wang, Wei-Ping,Zheng, Ya-Biao,Xiao, Juan-Juan,Zhang, Ping,Wang, Jian-Guo,Ashwani, Neetika,Ding, Wei-Liang,Jiang, Hua,Shang, Yan,Wang, Ming-Hua Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.13
Nogo protein, encoded by gene reticulon-4 (RTN4), includes three major isoforms by different splicing, named Nogo-A Nogo-B and Nogo-C. Nogo proteins play an important role in the apoptosis of cells, especially in tumor cells. RTN4 single nucleotide polymorphisms (SNPs) can influence the efficiency of transcription and translation thus being related with an individual's predisposition to cancer. The CAA insertion/deletion polymorphism (rs34917480) within RTN4 3'-UTR has been reported to be associated with many cancer types. In order to investigate the relationship between this polymorphism and susceptibility to non-small cell lung cancer (NSCLC) in the Chinese population, we conducted the present case-control study including 411 NSCLC patients and 471 unrelated healthy controls. The genotype distributions were significantly different between cases and controls (p=0.014). We found that the del allele could significantly increase NSCLC risk (ins/ins vs ins/del: p=0.007, OR 1.46, 95%CI=1.11-1.93; dominant model: p=0.004, OR 1.47, 95%CI=1.13-1.92 and allele model: p=0.008, OR 1.35, 95%CI=1.08-1.67). This association was stronger in participants over 60 years old, males and smokers. We therefore conclude that the CAA insertion/deletion polymorphism (rs34917480) contributes to non-small cell lung cancer risk in Chinese population. Age, sex and environmental exposure are also related to carcinogenic effects of rs34917480.
JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis
Li Xie,Hui Chen,Li Zhang,Yue Ma,Yuan Zhou,Yong-Yu Yang,Chang Liu,Yu-Li Wang,Ya-Jun Yan,Jia Ding,Xiao Teng,Qiang Yang,Xiu-Ping Liu,Jian Wu 대한간학회 2024 Clinical and Molecular Hepatology(대한간학회지) Vol.30 No.2
Background/Aims: Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet. Methods: Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation. Results: In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL. Conclusions: JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.