• KSBB Journal
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• v.18 no.5
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• pp.424-428
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• 2003

In the present study, we have analyzed effects of the endocrine distruptors, such as bisphenol A, nonylphenol and pentachlorophenol, on cell proliferation in the human breast cancer cell line, MCF-7, and the human prostate cancer cell line, PC-3, with MTT method. A dose dependent analysis of the cell proliferation of MCF-7 cells after administration of bisphenol A, nonylphenol and pentachlorophenol revealed a significant induction of cell proliferation. Maximum induction of cell proliferation was observed at concentrations between 10$\^$-7/ and 10$\^$-6/ M. Whereas, these chemicals had little effect on proliferation of PC-3 cells. These results demonstrated that bisphenol A, nonylphenol and pentachlorophenol do not induce proliferation of PC-3 cells but exhibit a significant induction of MCF-7 cell proliferation, suggesting all these chemicals are a estrogen mimic.

• Journal of Gastric Cancer
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• v.6 no.3
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• pp.132-138
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• 2006

Purpose: Dopamine is a neurotransmitter, but in the GIT, the roles of dopamine are a regulator of epithelial cell proliferation, an endogenous protective factor, and a regulator of stomach cancer cell proliferation. By using two different gastric-cancer cell lines, we assessed the effects of dopamine and dopamine receptors on the proliferation of human gastric-cancer cells. Materials and Methods: To assess the effects of dopamine and dopamine receptors on the proliferation of human gastric-cancer cells, we investigated cell proliferation and the expression of D1, D2L, and D2S receptor in two gastric-cancer cell lines, SNU 601 and KCU-C2. The effects of dopamine and dopamine receptors on the level of the cell proliferation were determined by staining with an A/H/E (acridine orange, hoechst and ethidium bromide) mixture. Results: After dopamine treatment, the cell viability was significantly decreased in SNU 601 cells (P<0.05) where the D2L receptor was absent, but not in KCU-C2 cells. After treatment with raclopride, a D2 receptor antagonist, dopamine-dose-dependent inhibition of cell proliferation was observed in SNU 601 cells (P<0.05). After treatment with SCH 23390, a D1 receptor antagonist, dopamine significantly increased ceil proliferation in KCU-C2 cells (P<0.05), but inhibited ceil proliferation in SNU 601 cells (no D2L receptor). Conclusion: The dopamine signal via the D1 or the D2S receptor inhibited proliferation of gastric-cancer cells, but that via the D2L receptor increased proliferation. These results suggest that the regulatory effects of dopamine in the gastric-cancer cell proliferation may be controlled by using dopamine receptors.

• Toxicological Research
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• v.11 no.1
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• pp.127-131
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• 1995

Sequential changes in cell proliferation during the development of epitherial kidney tumors induced in rats were investigated by autoradiographic determination of the $^3H$-thymidine-labeling index. Renal cell tumors were induced in male Sprague-Dawley rats by oral administration of N-nitrosomorpholine at the concentration of 120 mg/l in the drinking water for 7 weeks. At different times between 12 and 34 weeks after withdrawal of the carcinogen (stop model) animals were sacrificed. According to cytological criteria, neoplastic lesions were classified into clear cell, acidophilic cell, basophilic cell and oncocytic tumors. The labeling index was found to be increased in all types of preneoplastic tubules as compared to their corresponding original tubules. A much stronger elevation of cell proliferation was ocurred during the development of renal cell tumors from preneoplastic tubules. Of four tumor types, acidophilic cell tumor showed the highest labeling index while oncocytoma exhibited the lowest proliferative activity. These findings are in good accordance with the clinical observations that acidophilic cell tumors have a worse prognosis than oncocytoma. The data presented in this study suggest that the individual proliferation rates may be an objective biological marker of kidney tumor aggressiveness.

• Molecules and Cells
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• v.24 no.3
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• pp.424-430
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• 2007

The biological effects of low-dose radiation have been investigated and debated for more than a century, but its cellular effects and regulatory mechanisms remain poorly understood. This study shows the human cellular responses to low-dose radiation in CCD-18 Lu cells, which are derived from normal human lung fibroblasts. We examined a colony-forming assay for cell survival by ionizing radiation. Live cell counting and cell cycle analysis were measured for cell proliferation and cell cycle progression following low-dose irradiation. We examined Raf and Akt phosphorylation to determine the proliferation mechanism resulting from low-dose radiation. We also observed that p53 and p21 were related to cell cycle response. We found that 0.05 Gy of ionizing radiation enhanced cell proliferation and did not change the progression of the cell cycle. In addition, 0.05 Gy of ionizing radiation transiently activated Raf and Akt, but did not change phospho-p53, p53 and p21 in CCD-18 Lu cells. However, 2 Gy of ionizing radiation induced cell cycle arrest, phosphorylation of p53, and expression of p53 and p21. The phosphorylation of Raf and Akt proteins induced by 0.05 Gy of ionizing radiation was abolished by pre-treatment with an EGFR inhibitor, AG1478, or a PI3k inhibitor, LY294002. Cell proliferation stimulated by 0.05 Gy of ionizing radiation was blocked by the suppression of Raf and Akt phosphorylation with these inhibitors. These results suggest that 0.05 Gy of ionizing radiation stimulates cell proliferation through the transient activation of Raf and Akt in CCD-18 Lu cells.

• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4775-4778
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• 2013

The key signaling networks regulating cancer cell proliferation remain to be defined. The leucine-rich repeat containing G-protein coupled receptor 48 (GPR48) plays an important role in multiple organ development. In the present study, we investigated whether GPR48 functions in cancer cells using MCF-7, HepG2, NCI-N87 and PC-3 cells. We found that GPR48 overexpression promotes while its knockdown using small interfering RNA oligos inhibits cell proliferation. In addition, Wnt/${\beta}$-catenin signaling was activated in cells overexpressing GPR48. Therefore, our results indicated that GPR48 activates Wnt/${\beta}$-catenin signaling to regulate cancer cell proliferation.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.8
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• pp.4907-4911
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• 2013

The key signaling networks regulating glioma cell proliferation remain poorly defined. The leucine-rich repeat containing G-protein coupled receptor 4 (Lgr4) has been implicated in intestinal, gastric, and epidermal cell functions. We investigated whether Lgr4 functions in glioma cells and found that Lgr4 expression was significantly increased in glioma tissues. In addition, Lgr4 overexpression promoted while its knockdown using small interfering RNA oligos inhibited glioma cell proliferation. In addition, Wnt/${\beta}$-catenin signaling was activated in cells overexpressing Lgr4. Therefore, our results revealed that Lgr4 activates Wnt/${\beta}$-catenin signaling to regulate glioma cell proliferation.

• IMMUNE NETWORK
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• v.15 no.4
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• pp.199-205
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• 2015

T-bet is a critical transcription factor that regulates differentiation of Th1 cells from $CD4^+$ precursor cells. Since T-bet directly binds to the promoter of the IFN-${\gamma}$ gene and activates its transcription, T-bet deficiency impairs IFN-${\gamma}$ production in Th1 cells. Interestingly, T-bet-deficient Th cells also display substantially augmented the production of IL-2, a T cell growth factor. Exogenous expression of T-bet in T-bet deficient Th cells rescued the IFN-${\gamma}$ production and suppressed IL-2 expression. IFN-${\gamma}$ and IL-2 reciprocally regulate Th cell proliferation following TCR stimulation. Therefore, we examined the effect of T-bet on Th cell proliferation and found that T-bet deficiency significantly enhanced Th cell proliferation under non-skewing, Th1-skewing, and Th2-skewing conditions. By using IFN-${\gamma}$-null mice to eliminate the anti-proliferative effect of IFN-${\gamma}$, T-bet deficiency still enhanced Th cell proliferation under both Th1- and Th2-skewing conditions. Since the anti-proliferative activity of T-bet may be influenced by IL-2 suppression in Th cells, we examined whether T-bet modulates IL-2-independent cell proliferation in a non-T cell population. We demonstrated that T-bet expression induced by ecdysone treatment in human embryonic kidney (HEK) cells increased IFN-${\gamma}$ promoter activity in a dose dependent manner, and sustained T-bet expression considerably decreased cell proliferation in HEK cells. Although the molecular mechanisms underlying anti-proliferative activity of T-bet remain to be elucidated, T-bet may directly suppress cell proliferation in an IFN-${\gamma}$- or an IL-2-independent manner.

• Journal of Korean Neurosurgical Society
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• v.64 no.5
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• pp.716-725
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• 2021

Objective : The anti-tumor effect of the beta-adrenergic receptor antagonist propranolol in breast cancer is well known; however, its activity in glioblastoma is not well-evaluated. The Notch-Hes pathway is known to regulate cell differentiation, proliferation, and apoptosis. We investigated the effect of propranolol to human glioblastoma cell lines, and the role of Notch and Hes signaling in this process. Methods : We performed immunohistochemical staining on 31 surgically resected primary human glioblastoma tissues. We also used glioblastoma cell lines of U87-MG, LN229, and neuroblastoma cell line of SH-SY5Y in this study. The effect of propranolol and isoproterenol on cell proliferation was evaluated using the MTT assay (absorbance 570 nm). The impact of propranolol on gene expression (Notch and Hes) was evaluated using real-time polymerase chain reaction (RT-PCR, whereas protein levels of Notch1 and Hes1 were measured using Western blotting (WB), simultaneously. Small interfering RNA (siRNA) was used to suppress the Notch gene to investigate its role in the proliferation of glioblastoma. Results : Propranolol and isoproterenol caused a dose-dependent decrease in cell proliferation (MTT assay). RT-PCR showed an increase in Notch1 and Hes1 expression by propranolol, whereas WB demonstrated increase in Notch1 protein, but a decrease in Hes1 by propranolol. The proliferation of U87-MG and LN229 was not significantly suppressed after transfection with Notch siRNA. Conclusion : These results demonstrated that propranolol suppressed the proliferation of glioblastoma cell lines and neuroblastoma cell line, and Hes1 was more closely involved than Notch1 was in glioblastoma proliferation.

• Journal of the Korean Academy of Clinical Electrophysiology
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• v.3 no.1
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• pp.13-29
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• 2005

This study was performed to examine the effects of therapeutic doses of ultrasound on cell migration distance and proliferation of biopsies from articular cartilage. Articular cartilage biopsies were isolated from proximal part of the tibial of chicken, and cultured. Cartilage explants were exposed for a single 5 min to ultrasound with $0.1{\sim}1.6\;W/cm^2$ (spatial average-temporal average) at a frequency of 1 MHz. A control group was treated with the ultrasound generator switched off. The cell migration distance and cell proliferation analysis were performed on day 6 after stimulation of ultrasound. The results revealed that ultrasound influenced cell migration distance and cell proliferation in intensity-dependent manner. It was found that ultrasounds at $0.2\;W/cm^2$, $0.4\;W/cm^2$, and $0.8\;W/cm^2$ were significantly increase respectively both cell migration distance and cell proliferation (p<0.05). However, cell migration distance and cell proliferation were not affected by exposure ultrasound at $0.1\;W/cm^2$ and $1.6\;W/cm^2$ compared with control group. These results suggest that low-intensity ultrasounds at $0.2\;W/cm^2$, $0.4\;W/cm^2$, and $0.8\;W/cm^2$ may stimulate cell proliferation of the chondroblasts, and reflect a potential role in cartilage repair.