• Natural Product Sciences
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• v.13 no.2
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• pp.123-127
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• 2007

We investigated effect of small black soybean fraction (SBSF) T cell-mediated responses for tumor surveillance and proliferation in leukemia cells in vitro. Each SBSF butanol fraction (SBSFBu) and SBSF chloroform fraction (SBSFCh) was administered p.o. once a day far 21 days in BALB/c mice and then levels of serum cytokines and subpopulation of lymphocytes were measured. Moreover, SBSF fraction was treated into the cultured various cell lines for proliferation in leukemia cell lines, NO production by RAW264.7 cells, and expression of p53 gene in U937 leukemia cells. These results showed that SBSFBu increased levels of serum IL-4but not IL-2 and IFN-${\gamma}$, and increased expression of CD4$^+$ T cells and CD8$^+$ T cells in splenocytes in vivo, while SBSFCh increased levels of serum IL-2 and IFN-${\gamma}$ but decreased IL-4, and increased CD8$^+$ T cells but not CD4$^+$ T cells. Moreover, both of SBSFBu and SBSFCh inhibited proliferation of HL60, U937, and L1210 leukemia cell lines in a dose-dependent manner, up-regulated NO production by RAW264.7 cells in a dose-dependent manner, and enhanced expression of p53 gene in U937 leukemia cells. Our findings indicate that SBSFBu and SBSFCh may enhance T cell-dependent immune responses, and that both of SBSFBu and SBSFCh may inhibit proliferation of leukemia cells by up-regulation of NO production and expression of p53 gene.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1993.05a
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• pp.84-84
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• 1993

Overexpression of the mutant p53, derived from mutation of the p53 gene which is located on the short arm of chromosome 17 and plays a role in suppression of the tumor, was reported in some human malignancy such as breast or colon carcinoma and suggested to be a prognostic factor. The authors investigated expression of p53 protein by immunohistochemical staining using anti-p53 monoclonal antibody in the paraffin embedded blocks of the 23 patients who were diagnosed at Seoul National University Hospital as adenoid cystic carcinoma of the head and neck between 1982 and 1991, and could be followed-up. 7 cases(34%) out of the 23 cases showed p53 expression, and there was no significant association between p53 positivity and local recurrence(p=0.31) or distant metastasis(p=0.16)

• Molecules and Cells
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• v.43 no.4
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• pp.397-407
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• 2020

DNAJB9 is known to be a member of the molecular chaperone gene family, whose cellular function has not yet been fully characterized. Here, we investigated the cellular function of DNAJB9 under strong mitogenic signals. We found that DNAJB9 inhibits p53-dependent oncogene-induced senescence (OIS) and induces neoplastic transformation under oncogenic RAS activation in mouse primary fibroblasts. In addition, we observed that DNAJB9 interacts physically with p53 under oncogenic RAS activation and that the p53-interacting region of DNAJB9 is critical for the inhibition of p53-dependent OIS and induction of neoplastic transformation by DNAJB9. These results suggest that DNAJB9 induces cell transformation under strong mitogenic signals, which is attributable to the inhibition of p53-dependent OIS by physical interactions with p53. This study might contribute to our understanding of the cellular function of DNAJB9 and the molecular basis of cell transformation.

• Parasites, Hosts and Diseases
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• v.53 no.3
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• pp.335-339
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• 2015

Cryptosporidium andersoni ATP-binding cassette (CaABC) is an important membrane protein involved in substrate transport across the membrane. In this research, the nucleotide binding domain (NBD) of CaABC gene was amplified by PCR, and the eukaryotic expression vector of pEGFP-C1-CaNBD was reconstructed. Then, the recombinant plasmid of pEGFP-C1-CaNBD was transformed into the mouse intestinal epithelial cells (IECs) to study the iron transportation function of CaABC. The results indicated that NBD region of CaABC gene can significantly elevate the transport efficiency of $Ca^{2+}$, $Mg^{2+}$, $K^+$, and $HCO_3{^-}$ in IECs (P<0.05). The significance of this study is to find the ATPase inhibitors for NBD region of CaABC gene and to inhibit ATP binding and nutrient transport of CaABC transporter. Thus, C. andersoni will be killed by inhibition of nutrient uptake. This will open up a new way for treatment of cryptosporidiosis.

• Korean Journal of Clinical Laboratory Science
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• v.39 no.3
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• pp.231-240
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• 2007

It has been reported the higher incidence rate of gastric cancer in our country. Helicobacter pylori (H. pylori), that exhibited a higher infection rate among Korean people, has been known as a cofactor to cause cancer. Therefore, the aim of this study was to identify correlations among overexpressions of COX-2 (Cyclooxygenase-2) gene, p53 mutation and cell proliferation index related to H. pylori. Taking 28 cases of gastric cancer with H. pylori detection, immunohistochemical staining for COX-2, p53 and Ki-67 were performed. In the H. pylori positive group, the well differentiated type and diffuse type of gastric cancer were distributed in larger area and the expression rate of COX-2 was revealed high. The H. pylori negative group showed higher p53 expression than that of the positive group. However, the statistical correlation between H. pylori and histopathological factors was not observed. The significantly higher expression of COX-2 had were observed in both well differentiated type and the intestinal type of gastric cancer. Although there were no statistical significances, this showed a higher inclination of manifest in the early gastric cancer. p53 exhibited a higher tendency of expression in the well differentiated, moderately differentiated and the intestinal type of gastric cancers including the early gastric cancer. Ki-67 was expressed in a significantly higher fashion along with the increase of age. In addition, it was significantly expressed in well differentiated type and intestinal type of gastric cancer. Therefore, these results suggest that H. pylori, COX-2, p53, and Ki-67 influences on the new occurrence of gastric cancer and its development procedures. In the future, the more researches would be required to focus on a larger category relative to gene expressions in gastric cancer.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.6
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• pp.1024-1030
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• 1996

Capsaicin (8-methyl-N-vanillyl-6-nonenamide: CAP) is a mai or ingredient of hot pepper that has been used as a spicy food additive, preservative, and medicine. In this study, we evaluated the effect of dietary CAP on the selected proto-oncogene(c-jun, c-myc, H-ras, erbB, p53) expressions in various tissues of mice. Male ICR mice were divided into four groups and fed the experimental diets containing CAP at the levels of 0, 5, 20 and 100ppm for four weeks. Steady state RNA levels in various tissues were measured by slot blot hybridization assay. C-jun expression level was enhanced in stomach tissue from mice fed 20ppm CAP and significantly reduced from mice fed 100ppm CAP. The c-jun expression levels were differentially altered in organ-specific manner, Tumor suppressor gene p53 expression level appeared to be slightly increased in the liver from mice fed 20ppm CAP. These results suggested that dietary CAP differentially modulates c-jun and p53 expression in various organs.

• The Journal of Korean Medicine
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• v.19 no.1
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• pp.145-164
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• 1998

The purpose of this study is to evaluate the effect of Injinchunggantang-derivative on proliferation of hepatocyte in rats. Cell viability is studied by MTI assay. The gene related to cell replication such as p53, waf1, bcl-2 and $bcl-_{X_L}$ is quantitized by quantitative RT-PCR and the proteins coded by these genes are studied by Western blotting. The results are as follows. 1. The hepatocytes cultured in medium with lnjinchunggantang-derivative showed better viability compared with control grroup in MTI assay, and the hepatocytes cultured in medium with the Injinchunggantang-derivative-and-ethanol-mixed group showed better viability than the hepatocytes cultrued in 10% ethanol culture medium(control group), noting that Injinchunggantang-derivative has protective effect on hepatocyte injury. There was no dose- and time-dependence. 2. In quantitative RT-PCR, i) Bel-2 gene increased significantly both in Injinchunggantang-derivative group and in Injinchunggantang-derivative-and-ethanol-mixed group, while it showed no significant increase or decrease in other group. ii) $Bcl-_{X_L}$ gene increased significantly in Injinchunggantang-derivative group as well as in Injinchunggantang-deri vative-and-ethanol -mixed group. iii) P53 gene showed no significant increase or decrease in hepatocytes cultured in medium with 10% ethanol and in hepatocytes cultured in medium with Injinchunggantang-derivative-and-ethanol-mixed group, suggesting that 10% ethanol induced cell toxicity, thus increased p53 gene expression. iv) Wafl gene showed no significant increase or decrease in hepatocytes cutured in medium with Injinchtrnggantang-derivative, while increased in hepatocytes cultured in medium with 10% ethanol and in hepatocytes cultured in medium with Injinchtrnggantang-derivative-andethanol-mixed group, suggesting that 10% ethanol induced cell toxicity increased wafl gene expression. 3. In the study on protein by western blotting, the band of bcl-2 and $bcl-_{X_L}$ were widened in Injinchtrnggantang-derivative group. Especially the amount of $bcl-_{X_L}$ increased significantly compared with other groups. But in the study on p53 and wafl, there was no significant difference among those groups. Above study shows that Injinchunggantang-derivative has good effect on cell viability and that the genes resistant to cell death such as bcl-2 and $bcl-_{X_L}$ are induced by Injinchunggantang-derivative to resist to cell death by toxic agent And this is reconfirmed in protein study using' western blotting: These results suggest that Injinchunggantang-derivative has inhibitory effect on cell death as well as protective effect on hepatocyte. Therefore this prescription is recommended in various liver diseases such as chronic liver disease and-induced hepatic injury.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7737-7741
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• 2013

Background: Human papilloma virus infection is associated with genesis and malignant potential of cervical cancer. E6 and E7 oncogens are known to bind to p53 and retinoblastoma gene products, abrogating their functions as tumor suppressors, leading to an abnormal cell cycle machinery. Roles of the p53 homolog p63 have also been postulated, E6 expression leading to TAp63b degradation allowing anchorage independent growth. Molecular studies correlated with clinicopathological factors are important to determine prognosis and treatment strategies, but results have been controversial and need to be clarified. Aim: To investigate expression of p53 and p63 in cervical squamous cell carcinomas in correlation with age, FIGO staging, morphology, and cancer cell proliferation. Materials and Methods: Expression of p53 and p63 immunohistochemical staining in a total of 56 paraffin-embedded tissues of cervical squamous cell carcinomas from Dr. Sardjito General Hospital Indonesia, was evaluated for correlation with clinicopathological parameters. The Mann-Whitney test was used to compare the percentage of p53 and p63 expression with patient age, FIGO staging and morphology and to compare mean p53 and p63 expression. The Spearman correlation test was applied to correlate p53 and p63 expression with that of Ki-67. A p-value of <0.05 was considered statistically significant. Results: There were significant associations between p53 expression with age (p=0.019) and FIGO staging (p=0.026), but not with with morphology or Ki-67 expression. There were no links between p63 expression and age, morphology, FIGO staging or Ki-67. Conclusions: This study indicated that p53 has a prognostic value in cervical squamous cell carcinomas given the relation with FIGO staging.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.83-83
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• 2003

Mutations of p53 tumor suppressor gene have been associated with exposure to carcinogens. Cultured human breast epithelial cells (MCF10A) were treated with Benzo(a)pyrene(BaP) or N-Methyl-N'-nitro-N-nitrosoguanidine(MNNG). MCF10A cells were grown in DMEM/F12 medium and trated for 6, 12, 24, 48 and 96h with Bap (1, 10 and 100 $\mu$M) dissolved in dimethylsulfoxide(DMSO). (omitted)

• Journal of Life Science
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• v.31 no.4
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• pp.400-409
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• 2021

Sanguinarine, a natural benzophenanthridine alkaloid, has been considered a potential therapeutic target for the treatment of cancer because it can induce apoptosis in human cancer cells; however, the underlying mechanisms of action still remain unclear. Tumor suppressor p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to anticancer agents. Therefore, in the present study, the role of p53 during apoptosis induced by sanguinarine was investigated in p53wild type (WT, p53+/+) and p53null (p53+/+) HCT116 colon carcinoma cells. Sanguinarine significantly caused greater reductions in cell viability in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells. Consistently, sanguinarine promoted more DNA damage and apoptosis in HCT116 (p53+/+) cells than in HCT116 (p53-/-) cells while increasing the expression of p53 and cyclin-dependent kinase inhibitor p21^WAF1/CIP1. Sanguinarine increased the activity of caspase-8 and caspase-9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and it activated caspase-3, a typical effect caspase, in HCT116 (p53+/+) cells. Sanguinarine also increased the generation of reactive oxygen species (ROS), and the Bax/Bcl-2 ratio, while destroying the integrity of mitochondria in HCT116 (p53+/+) cells, but not in HCT116 (p53-/-) cells. Overall, the results indicate that sanguinarine induced p53-dependent apoptosis through ROS-mediated activation of extrinsic and intrinsic apoptotic pathways in HCT116 colorectal cancer cells.