• KSBB Journal
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• 제18권5호
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• pp.424-428
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• 2003

내분비계장애물질인 bisphenol A, nonylphenol, pentachlorophenol을 대상으로 여성 유방암세포 유래 MCF-7 세포주와 남성 전립선암세포 유래 PC-3 세포주에서 세포 증식효과를 MTT 방법으로 조사하였다. MCF-7 세포주에 이들 세 종류의 내분비계장애물질을 농도별로 처리하여 세포증식에 미치는 영향을 조사한 결과 모두 세포증식을 촉진하는 결과를 보였다. $10^{-7}$ M에서 $10^{-6}$ M 농도 범위에서 MCF-7 세포의 최대증식효과를 유도하였다. 그러나 PC-3 세포주의 경우에는 세포증식에 bisphenol A, nonylphenol, pentachlorophenol 모두 영향을 미치지 못하였다. 이러한 결과는 이들 세 종류의 내분비계 장애물질이 남성 전립선세포 유래인 PC-3 세포주의 증식에는 관여하지 않고 여성 유방암 세포에서 유래하고 에스트로젠 반응성인 MCF-7 세포주에만 증식효과를 갖는 사실을 보여주고 있으며 이는 bisphenol A, nonylphenol, pentachlorophenol이 여성호르몬인 에스트로젠과 유사한 역할을 한다는 사실을 보여주는 것이라 할 수 있다.

• Journal of Microbiology and Biotechnology
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• 제30권7호
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• pp.1044-1050
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• 2020

Abelmoschus manihot (Linn.) is a medicinal herbal plant that is commonly used to treat chronic kidney disease and hepatitis. However, its effect on cell proliferation has not been clearly revealed. In this report, we sought to determine the effect of the flower extract of A. manihot (FA) on cell proliferation. Based on our findings, FA increased the proliferation of human diploid fibroblast (HDF) and HEK293 cells. Through cell cycle analysis, FA was found to increase the number of HDF cells in the S phase and G2/M phase. FA also increased the expression of cyclin D1 and enhanced the migration of HDF cells. By administering FA to HDF cells with ≥30 passages, a decrease in the number of senescence-associated β galactosidase-positive cells was observed, thereby indicating that FA can ameliorate cellular senescence. Collectively, our findings indicate that FA increases cyclin D1 expression and regulates cell proliferation.

• 한방안이비인후피부과학회지
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• 제12권1호
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• pp.79-98
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• 1999

The purpose of this Study was to investigate effect of TakliSodokSan(TSS) on the anti-tumor, immunocytes and nitric oxide(NO) production from mice peritoneal macrophages. This Study estimated the proliferation of L1210 cell lines, A431 cell lines, Hep-G2 cell lines, K562 cell lines, 3T3 cell lines, mouse thymocytes and mouse splenocytes and NO production from pcritoneal macrophages in vitro, and estimated the proliferation of L1210 cells, thymocytes and splenocytcs, NO production from peritoneal macrophages and body weight in L1210 cells-transplanted mice in vivo. The results were obtained as follows; 1. TSS inhibited significantly the proliferation of L1210, A431, Hep-G2, K562 cell lines in vitro. 2. TSS accelerated the proliferation of mice thymocytes and splenocytes in vitro. 3. TSS was not increased the nitric oxide production from mice peritoneal macrophages in vitro. 4. TSS inhibited significantly the proliferation of L1210 cells in Ll210 cells∼transplanted mice. 5. TSS accelerated the proliferation of mice thymocytes and splenocytes In L1210 cells-transplanted mice. 6. TSS was increased significantly the nitric oxide production from mice peritoneal macrophages in L1210 cells-transplanted mice. 7. TSS was increased the body weight as comparing with control group in Ll210 cells-transplanted mice.

• Journal of Nutrition and Health
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• 제34권8호
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• pp.896-904
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• 2001

Conjugated linoleic acid(CLA) is a group of positional and geometric isomers of linoleic acid(LA) and exhibits anticarcinogenic activity in multiple experimental animal models. Cis-9,trns-11(c9t11) and trans-10,cis-12(t10c12) CLA are the principal isomers found in foods. The present study was performed to determine whether CLA and the two isomers inhibits HT-29 cell proliferation and to assess whether such an effect was related to changes in secretion of eicosanoids. Cells were incubated in serum-free medium with various concentrations(0 to 20$\mu$M) of CLA or LA. CLA inhibited cell proliferation in a dose-dependent manner, with maximal inhibition(70 $\pm$ 1%) observed at 20$\mu$M concentration after 96 hours. However, LA had no effect at the same concentration range. To compare the ability of c9f11 and t10c12 to inhibit cell proliferation, cells were incubated with increasing concentrations(0 to 4$\mu$M) of these isomers. T10c12 inhibited cell proliferation in a dose-dependent manner. A 66 $\pm$ 2% decrease in cell number was observed within 96 hours after addition of 4$\mu$M t10c12. By contrast, c9t11 had no effect. The concentrations of CLA and the two isomers in the plasma membrane were increased when they were added to the incubation medium. However, they did not alter the levels of arachidonic acid in plasma membrane. To assess whether the proliferation inhibiting effect of CLA was related to changes in eicosanoid production, prostaglandin E$_2$(PGE$_2$) and leukotriene B$_4$(LTB$_4$) concentrations in conditioned media were estimated by a competitive enzyme immunoassay. Both CLA and t10c12 increased the production of materials reactive to PGE$_2$ and LTB$_4$ antibodies in a dose-dependent manner. By contrast, c9t11 had no effect. These results indicate that inhibition of HT-29 cell proliferation by CLA is attributed to the effect of the t10v12 isomer. The materials reactive to PGE$_2$ and LTB$_4$ antibodies may inhibit growth stimulatory effect of arachidonic acid-derived eicosanoids on HT-29 cell proliferation.

• 동의생리병리학회지
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• 제18권1호
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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.

• IMMUNE NETWORK
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• 제15권4호
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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 Nutrition and Health
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• 제31권1호
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• pp.21-27
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• 1998

The objective of this study was to observe the effect of dietary calcium(Ca) level on colonic mucosal levels of cell proliferation, 1, 2-diacylglycerol(DAG), TXB2, PGE2 and phospholipid fatty acid composition which have been known as biomarkers for colon cancer. One hundred male Sprague Dawley rats, at 7 weeks of age, were divided into two fat type groups. Each group of which was further divided into two Ca level groups. Each rt was intramuscularly injected with 1, 2,-dimenthylhydrazine(DMH) for 6 weeks (total dose of 180mg/kg body weight) and simultaneously fed one of four experimental diets containing 15% dietary fat(corn oil or perilla oil )and 0.3% or 1.0% Ca by weight for 20 weeks. Compared to corn oil, perilla oil significantly reduced cell proliferation by decreasing labeling index, proliferating zone, crypt length in colonic mucosa and colonic mucosa and colonic mucosal levels of DAG, TXB2 . PGE2 and phospolipid (PL) arachidonic acid distribution. The effect of Ca on biomarketrs was different depending on the type of dietary fat comsumed . Ca effect of Ca on biomarkers was different depending on the type of dietary fat comsumed. Ca effect was not significantly shown in the PO group, but it was significant in the CO group in which high Ca(1.0%) decreased the levels of levels of PL-C20 : 4(%), DAG and PGE2 . However , high Ca supplementation had shown only the trends of improving cell proliferation. Overall , high dietary Ca significantly reduced cell proliferation by inhibiting the synthesis of eicosanoid and DAG with reduced distribution of PL-C20 : 4 , which may have resulted in lower activation of PKC through reduced signal transduction. Since a high level of dietary Ca was more effective in reducing the risk factor against colon cancer in corn oil fed rats, it could be suggested that a higher amount of dietary Ca be consumed , especially when more vegetable oil rich in linoleic acid is included in the diet.

• 한국축산식품학회지
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• 제25권2호
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• pp.244-249
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• 2005

To investigate the effect of Holstein colostrum peptide fraction on proliferation of immune cell, polypeptide fractions were separated from acid whey into 3 fractions depending on molecular weight by ultrafiltration: Fraction I, which contains the polypeptide larger than 10,000 Da, Fraction n, which contains the polypeptide ranging from 1,000 Da to 10,000 Da and Fraction III, which contains the polypeptide smaller than 1,000 Da. EL-4 cell (murine T lymphoma cell) was used to evaluate immune enhancing effect of each fraction from Holstein colostrum. Fraction n showed the highest proliferative effect of the colostrum whey fractions on EL-4 cell at 1mg/mL compared with whole whey and other fractions and this proliferative activity was shown in dose dependent manner. Fraction n showed the highest proliferative effect on PMA (Phorbol 12-myristate 13-acetate) stimulated EL-4 cell. Heated Fraction n showed similar effect to native one on proliferation of both EL-4 cell and PMA stimulated EL-4 cell.

• Asian Pacific Journal of Cancer Prevention
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• 제16권6호
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• pp.2397-2402
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• 2015

Previous studies have shown that miR-454 plays an important role in a variety of biological processes in various human cancer cells. However, the underlying mechanisms of this microRNA in colorectal cancer (CRC) cells remain largely unknown. In the present study, we investigated the miR-454 role in CRC cell proliferation. We found that miR-454 expression is markedly upregulated in CRC tissues and CRC cells compared with the matched tumor adjacent tissues and the FHC normal colonic cell line. Ectopic expression of miR-454 promoted the proliferation and anchorage-independent growth of CRC cells, whereas inhibition of miR-454 reduced this effect. Bioinformatics analysis further revealed cylindromatosis (CYLD), a putative tumor suppressor as a potential target of miR-454. Data from luciferase reporter assays showed that miR-454 directly binds to the 3'-untranslated region (3'-UTR) of CYLD mRNA and repressed expression at both transcriptional and translational levels. In functional assays, CYLD-silenced in miR-454-in-transfected SW480 cells have positive effect to promote cell proliferation, suggesting that direct CYLD downregulation is required for miR-454-induced CRC cell proliferation. In sum, our data provide compelling evidence that miR-454 functions as an onco-miRNA, playing a crucial role in the promoting cell proliferation in CRC, and its oncogenic effect is mediated chiefly through direct suppression of CYLD expression.

• Asian Pacific Journal of Cancer Prevention
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• 제13권3호
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• pp.1043-1048
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• 2012

The COPS3 gene has stimulating effect on cell proliferation and progression of osteosarcomas and related cells. However, the features of COPS3 and its potential application as a therapeutic target in other cancers has not yet been studied. In this study, therefore, the effect of COPS3 silencing via COPS3 siRNA on lung cancer cell proliferation was examined. Expression levels of COPS3 gene in COPS3 siRNA infected cells and control siRNA infected cells were compared with real time PCR and Western blot analysis. Cell proliferation levels were comprehensively analyzed by MTT, BrdU incorporationy, and colony formation assays. For mechanistic assessment the effects of COPS3 silencing on cell cycle and apoptosis were analyzed using flow cytometry. Results showed that successful silencing of the COPS3 gene at both translational and transcriptional levels significantly reduced the proliferation and colony formation by lung cancer cells (p<0.01). Flow cytometry showed cell cycle arrest in the G0/G1 phase after COPS3 silencing, and more importantly, apoptosis was induced as a result of COPS3 knockdown, which negatively affected cell survival. Therefore, these results provide another piece of important evidence that the COPS3 gene expressed in lung cancer cells may play a critical role in stimulating proliferation. Down-regulation of COPS3 could significantly inhibit lung cancer cell growth, which was most likely mediated via induction of cell cycle arrest in G0/G1 phase and apoptosis.