• Title, Summary, Keyword: cell proliferation

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Reactive Oxygen Species Co-Operated with Sex Hormones Inhibit Proliferation of Hepal-6 Cells

  • Wang Ai-Guo;Kim Nam-Soon;Lee Dong-Seok
    • Biomedical Science Letters
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    • v.11 no.3
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    • pp.253-258
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    • 2005
  • Reactive oxygen species (ROS) and sex hormones affect the proliferation of cells and are believed to play important roles in tumorigenesis. However, little is known regarding how these two factors interact to affect cell proliferation. In this study, hepal-6 cells were treated with ROS and sex hormones (testosterone and steroidal) either separately or in combination. The sex hormones had no significant influence the cell proliferation up to a concentration of $1{\mu}M$. However, cell proliferation was inhibited when the cells were treated simultaneously with $H_2O_2$, which alone was found to promote cell proliferation at the concentrations of $15{\mu}M$. In conclusion, this study indicates that instead of promoting the cell proliferation, ROS interact with sex hormones to inhibit the Hepa 1-6 cell proliferation.

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Effects of Exogenous ATP on Calcium Mobilization and Cell Proliferation in C6 Glioma Cell

  • Lee, Eun-Jung;Cha, Seok-Ho;Lee, Woon-Kyu;Lee, Kweon-Haeng;Lee, Sang-Bok
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.4
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    • pp.419-425
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    • 1998
  • To clarify the effect of extracellular ATP in cultured C6 glioma cells, ATP-induced cytosolic free calcium ($[Ca^{2+}]_i$) mobilization and cell proliferation were investigated. ATP-induced $[Ca^{2+}]_i$ increased in a dose-dependent manner $(10^{-7}\;M{\sim}10^{-3}\;M)$. ATP-induced $[Ca^{2+}]_i$ increases were slightly slowed in extracellular calcium-free conditions especially in sustained phase. ATP-induced $[Ca^{2+}]_i$ increment was also inhibited by the pretreatment of U73122, a phospholipase C (PLC) inhibitor, in a time-dependent manner. Suramin, a putative $P_{2Y}$ receptor antagonist, dose-dependently weakened ATP-induced $[Ca^{2+}]_i$ mobilization. Significant increases in cell proliferation were observed at 2, 3, and 4 days after ATP was added. Stimulated cell proliferation was also observed with adenosine at days 2 and 3. This cell proliferation was significantly inhibited by the treatment with suramin. Ionomycin also stimulated cell proliferation in a concentration-dependent manner. In conclusion, we suggest that extracellular ATP stimulates C6 glioma cell proliferation via intracellular free calcium mobilization mediated by purinoceptor.

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Acupuncture Suppresses Intrastriatal Hemorrhage-Induced Neuronal Cell Death and Proliferation in Rats

  • Cho, Nam-Hun;Park, Dong-suk;Lee, Jae-Dong
    • The Journal of Korean Medicine
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    • v.24 no.4
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    • pp.127-135
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    • 2003
  • Objectives : Intracerebral hemorrhage (ICH) is one of the most devastating types of stroke. The effect of acupuncture on the intrastriatal hemorrhage-induced neuronal cell death and cell proliferation in rats is examined. Methods : Cell death and cell proliferation in rats was investigated via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and immunohistochemistry for caspase-3 and 5-bromo-2'-deoxyuridine (BrdU). Results : Results showed that apoptotic cell death in the striatum and cell proliferation in the hippocampal dentate gyrus significantly increased following intrastriatal hemorrhage in rats, and that acupunctural treatment at the Zusanli acupoint suppressed the hemorrhage-induced increase in apoptosis in the striatum and cell proliferation in the dentate gyrus. Conclusions : It is suggested that acupunctural treatment, especially at the Zusanli acupoint, may aid recovery following central nervous system sequelae following ICH.

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Bee Venom Suppresses Ischemia-induced Increment of Apoptosis and Cell Proliferation in Hippocampal Dentate Gyrus

  • Lim Baek Vin;Lee Choong Yeol;Kang Jin Oh;Kim Chang Ju;Cho Sonhae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.1
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    • pp.236-242
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    • 2004
  • Cerebral ischemia resulting from transient or permanent occlusion of cerebral arteries leads to neuronal cell death and eventually causes neurological impairments. Bee venom has been used for the treatment inflammatory disease. In the present study, the effects of bee venom on apoptosis and cell proliferation in the hippocampal dentate gyrus following transient global ischemia in gerbils were investigated using immunohistochemistry for cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), caspase-3, and 5-bromo-2'-deoxyuridine (BrdU). It was shown that apoptotic cell death and cell proliferation in the hippocampal dentate gyrus were significantly increased following transient global ischemia in gerbils and that treatment of bee venom suppressed the ischemia-induced increase in apoptosis and cell proliferation in the dentate gyrus. The present results also showed that 1 mg/kg bee-venom treatment suppressed the ischemia-induced increasing apoptosis, cell proliferation, and COX-2 expression in the dentate gyrus. It is possible that the suppression of cell proliferation is due to the reduction of apoptotic cell death by treatment of bee venom. In the present study, bee venom was shown to prosses anti-apoptotic effect in ischemic brain disease, and this protective effect of bee venom against ischemia-induced neuronal cell death is closely associated with suppression on caspase-3 expression.

miRNA-1297 Induces Cell Proliferation by Targeting Phosphatase and Tensin Homolog in Testicular Germ Cell Tumor Cells

  • Yang, Nian-Qin;Zhang, Jian;Tang, Qun-Ye;Guo, Jian-Ming;Wang, Guo-Min
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.15
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    • pp.6243-6246
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    • 2014
  • To investigate the role of miR-1297 and the tumor suppressor gene PTEN in cell proliferation of testicular germ cell tumors (TGCT). MTT assays were used to test the effect of miR-1297 on proliferation of the NCCIT testicular germ cell tumor cell line. In NCCIT cells, the expression of PTEN was assessed by Western blotting further. In order to confirm target association between miR-1297 and 3'-UTR of PTEN, a luciferase reporter activity assay was employed. Moreover, roles of PTEN in proliferation of NCCIT cells were evaluated by transfection of PTEN siRNA. Proliferation of NCCIT cells was promoted by miR-1297 in a concentration-dependent manner. In addition, miR-1297 could bind to the 3'-UTR of PTEN based on luciferase reporter activity assay, and reduced expression of PTEN at protein level was found. Proliferation of NCCIT cells was significantly enhanced after knockdown of PTEN by siRNA. miR-1297 as a potential oncogene could induce cell proliferation by targeting PTEN in NCCIT cells.

Contribution of RIZ1 to Regulation of Proliferation and Migration of a Liver Fluke-Related Cholangiocarcinoma Cell

  • Khaenam, Prasong;Niibori, Akiko;Okada, Seiji;Jearanaikoon, Patcharee;Araki, Norie;Limpaiboon, Temduang
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.8
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    • pp.4007-4011
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    • 2012
  • Purpose: Retinoblastoma-interacting zinc finger gene (RIZ1) is a tumor suppressor gene which is highly inactivated by promoter hypermethylation in patients with liver fluke-related cholangiocarcinoma (CCA). Epigenetic aberration of this gene might withdraw the ability to restrain tumor cell proliferation and migration. We aimed to define the role of RIZ1 on cell proliferation and migration in CCA cell line. Materials and methods: Small interference RNA (siRNA) was used to knock down the expression of RIZ1 in a CCA-derived cell line in which cell proliferation and cell migration were performed. Results: A predominant nuclear localization of RIZ1 was observed. Reduction of RIZ1 by siRNA augmented cell proliferation and migration. Conclusion: The result suggested that RIZ1 might play a role in regulating cell proliferation and migration in CCA. Reduction of RIZ1 expression may aggravate the progression of CCA.

Nuclear Imaging of Cellular Proliferation (핵의학적 세포증식 영상)

  • Yeo, Jeong-Seok
    • The Korean Journal of Nuclear Medicine
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    • v.38 no.2
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    • pp.198-204
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    • 2004
  • Tumor cell proliferation is considered to be a useful prognostic indicator of tumor aggressiveness and tumor response to therapy but in vitro measurement of individual proliferation is complex and tedious work. PET imaging provides a noninvasive approach to measure tumor growth rate in situ. Early approaches have used $^{18}F$-FDG or methionine to monitor proliferation status. These 2 tracers detect changes in glucose and amino acid metabolism, respectively, and therefore provide only an indirect measure of proliferation status. More recent studies have focused on DNA synthesis itself as a marker of cell proliferation. Cell lines and tissues with a high proliferation rate require high rates of DNA synthesis. $[^{11}C]Thymidine$ was the first radiotracer for noninvasive imaging of tumor proliferation. The short half-life of $^{11}C$ and rapid metabolism of $[^{11}C]Thymidine$ in vivo make the radiotracer less suitable for routing use. Halogenated thymidine analogs such as 5-iodo-2-deoxyuridine (IUdR) can be successfully used as cell proliferation markers for in vitro studies because these compounds are rapidly incorporated into newly synthesized DNA. IUdR has been evaluated as a potential in vivo tracer in nuclear medicing but the image qualify and the calculation of proliferation rates are impaired by its rapid in vivo degradation. Hence, the thymidine analog $3'-deoxy-3'-^{18}F-fluorothymidine$ (FLT) was recently introduced as a stable proliferation marker with a suitable nuclide half-life and stable in vivo. $[^{18}F]FLT$ is phosphorylated to 3-fluorothymidine monophosphate by thymidine kinase 1 and reflects thymidine kinase 1 activity in proliferating cell. $[^{18}F]FLT$ PET is feasible in clincal use and well correlates with cellular proliferation. Choline is a precursor for the biosynthesis of phospholipids (in particular, phosphatidylcholine), which is the essential component of all eukaryotic cell membranes and $[^{11}C]choline$, which is a new marker for cellular proliferation.

Exosomes Secreted by Toxoplasma gondii-Infected L6 Cells: Their Effects on Host Cell Proliferation and Cell Cycle Changes

  • Kim, Min Jae;Jung, Bong-Kwang;Cho, Jaeeun;Song, Hyemi;Pyo, Kyung-Ho;Lee, Ji Min;Kim, Min-Kyung;Chai, Jong-Yil
    • The Korean Journal of Parasitology
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    • v.54 no.2
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    • pp.147-154
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    • 2016
  • Toxoplasma gondii infection induces alteration of the host cell cycle and cell proliferation. These changes are not only seen in directly invaded host cells but also in neighboring cells. We tried to identify whether this alteration can be mediated by exosomes secreted by T. gondii-infected host cells. L6 cells, a rat myoblast cell line, and RH strain of T. gondii were selected for this study. L6 cells were infected with or without T. gondii to isolate exosomes. The cellular growth patterns were identified by cell counting with trypan blue under confocal microscopy, and cell cycle changes were investigated by flow cytometry. L6 cells infected with T. gondii showed decreased proliferation compared to uninfected L6 cells and revealed a tendency to stay at S or G2/M cell phase. The treatment of exosomes isolated from T. gondii-infected cells showed attenuation of cell proliferation and slight enhancement of S phase in L6 cells. The cell cycle alteration was not as obvious as reduction of the cell proliferation by the exosome treatment. These changes were transient and disappeared at 48 hr after the exosome treatment. Microarray analysis and web-based tools indicated that various exosomal miRNAs were crucial for the regulation of target genes related to cell proliferation. Collectively, our study demonstrated that the exosomes originating from T. gondii could change the host cell proliferation and alter the host cell cycle.

Role of Non-Thermal DBD Plasma on Cell Migration and Cell Proliferation in Wound Healing

  • Ali, Anser;Lee, Seung Hyun;Kim, Yong Hee;Uhm, Han Sup;Choi, Eun Ha;Park, Bong Joo
    • Proceedings of the Korean Vacuum Society Conference
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    • pp.526-526
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    • 2013
  • Plasma technology isbeing developed for a range of medical applications including wound healing. However, the effect of plasma on many cells and tissues is unclear. Cell migration and cell proliferation are very important biological processes which are affected by plasma exposure and might be a potential target for plasma therapy during wound healing treatment. In this study, we confirmed the plasma exposure time and incubation time after plasma treatment in skin fibroblast (L-929 cells) to evaluate the optimal conditions forplasma exposure to the cell in-vitro. In addition, we used a scratch method to generate artificial wound for evaluating the cell migration by plasma treatment. Where, the cells were treated with plasma and migration rate was observed by live-cell imaging device. To find the cell proliferation, cell viability assay was executed. The results of this study indicate the increased cell proliferation and migration on mild plasma treatment. The mechanisms for cell migration and cell proliferation after plasma treatment for future studies will be discussed.

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Losartan Inhibits Vascular Smooth Muscle Cell Proliferation through Activation of AMP-Activated Protein Kinase

  • Kim, Jung-Eun;Choi, Hyoung-Chul
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.5
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    • pp.299-304
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    • 2010
  • Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.