• BMB Reports
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• v.29 no.5
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• pp.484-487
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• 1996

The matrix metalloproteinases (MMPs) are members of a unique family of proteolytic enzymes that degrade components of the extracellular matrix. Significant evidence has accumulated to directly implicate members of the MMPs in tumor invasion and metastasis formation. To investigate the correlation between ras oncogene and MMP gene expression in various tumor cells, we detected mRNAs for the ras, MMP-2 and MMP-9 (72 kD and 92 kD type IV collagenases, respectively) genes in nine human tumor cell lines. The ras gene was expressed in seven cell lines; MMP-2 in three; MMP-9 in two cell lines tested. There was no direct correlation between the ras oncogene and MMP expression. A clear difference in the mRNA expression between MMP-2 and MMP-9 was observed among the cell lines. As an approach to study the effect of the ras oncogene on metastasis, we examined the expressions of MMP-2 and MMP-9 in HT1080 cells transfected with the v-H-ras gene. MMP-9 expression was Significantly enhanced in the ras-transfected HT1080 cells compared with the nontransfectants while ras transfection did not affect the expression of MMP-2. These results suggest the possible inducing effect of the ras oncogene on the metastasis by activation of the MMP-9 gene in HT1080.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.3
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• pp.743-752
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• 2012

Hepatocellular carcinoma is a common disorder worldwide which ranks 5th and 7th most common cancer among men and women. In recent years, different incidence trends have been observed in various regions, but the reasons are not completely understood. However, due to the great public efforts in HCC prevention and alternation of lifestyle, the roles of some well documented risk factors played in hepatocarcinogenesis might have changed. This paper summarizes both the environmental and host related risk factors of hepatocellular carcinoma including well established risk factors such as hepatitis virus infection, aflatoxin and alcohol, as well as possible risk factors such as coffee drinking and other dietary agents.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2003.10a
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• pp.40-40
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• 2003

The c-erbB2/neu oncogene (alias HER2, NEU) encoding a tyrosine kinase receptor protein, the overexpression of which correlates with a more rapid progression and a worse prognosis in human breast cancer [1]. Otherwise, this gene is still poorly investigated in veterinary oncology [2,3]. To gain insight into the patterns of c-erbB2/neu status in canine mammary tumor, we constructed one such mammary tumor tissue microarray (TMA) from 60 tumors from our lab. This enabled the amplification of c-erbB2/neu oncogene of all 60 tumors to be simultaneously analyzed by chromogenic in situ hybridization (CISH). The aim of this study was to evaluate status of c-erbB2/neu oncogene in canine mammary tumors and to correlate this status with the differentiation grade of neoplasm. (omitted)

• 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.

• Korean Journal of Biological Psychiatry
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• v.4 no.2
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• pp.211-217
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• 1997

The Bcl-2 protein has been shown to block apoptosis induced by a variety of stimuli. We have performed the experiments which cell death can be blocked by the bcl-2 proto-oncogene under moderate(50-100mM) or high ethanol treatment(400-600mM). As a result of morphological changes, and MTT assay, cell death was blocked by Bcl-2 under 100mM ethanol. However, the results of DNA fragmentation and RT-PCR(ICE, and CPP32), immunoblotting(CPP32, and PARP) for SK-pcDNA3 cells(vector only) and SK-Bcl-2 cells(stably expressed bcl-2 gene) were showen to be no significant differences between two cell lines. These results suggested that cell death induced by ethanol was not followed by apoptosis mechanism, and was blocked by the bcl-2 proto-oncogene with moderate ethanol.

• Journal of the Korean Society of Food Science and Nutrition
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• v.21 no.3
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• pp.314-318
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• 1992

The sarcoma 180 cells were treated with ursolic acid which was previously extracted from leaves of Eriobotrya japonica Lindy (Rosaceae) and identified as a potent anticarinogenic agent. Suppressing effects of the compounds with testing changes in selected oncogenes expression were examined by using the northern hybridization method. Ursolic acid significantly suppressed c-myc oncogene expression. However, c-ha-ras oncogene expression was lowered slightly with the ursolic acid treatment. Therefore, it was concluded that preproven anticarcinogenic effects of ursolic acid should be partly ascribed to the modified oncogenic expression.

• Journal of Life Science
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• v.19 no.9
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• pp.1289-1293
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• 2009

Proto-oncogene human cervical cancer oncogene (HCCR) functions as a negative regulator of p53 and contributes to tumorigenesis in various human tissues. However, it is unknown how HCCR contributes to the cellular and biochemical mechanisms of human tumorigenesis. In this study, we showed how the expression of HCCR is modulated. The luciferase activity assay indicated that the HCCR 5'-flanking region at positions -370 to -406 plays an important role in the promoter activity. Computational analysis of this region identified one consensus sequence for the TG-interacting factor (TGIF) located at -390 to -366 (TG). Mobility shift assays (EMSA) revealed that nuclear proteins from K562 bind to the TG site, but not to the mutated TG site. The reporter activity assay with promoter constructs carrying mutated TGIF sequences pGL3-mTGIF significantly increased reporter activities compared to wild type constructs pGL3-$406{\sim}+30$. In this study, we characterized the HCCR promoter and found that HCCR expression was partially regulated by the transcription repressor TGIF, which bound the promoter at positions -390 to -366.

• Journal of Korea Technology Innovation Society
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• v.15 no.2
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• pp.369-399
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• 2012

Purpose: Health technology research & development is an important area to leading future. This study examined the current trends for 'oncogene' based on the research subject network to deduce a research front. Method: Papers were extracted from PubMed database using MeSH term for studies on 'oncogenes' and further categorized as papers published by Korean. Keywords were collected from all of articles. Research subject network was generated by keywords. Research subject network was analyzed by weighted degree centrality based social network analysis and transition of research subjects was analyzed by the time series. Results: On 'oncogenes', 'Genes, ras', 'Apoptosis', 'Signal Transduction' had a high degree centrality and currently 'Antineoplastic Agents', 'Prognosis', and 'Tumor Markers, Biological' were widely conducted. Conclusion: Consistency of research trend pattern was found by analyzing oncogene network with compromised to international vs. domestic trends. Analyzing keyword networks in various subject area, those will allow us to predict the research progress and propose evidence of research & developmental strategy.

• Genomics & Informatics
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• v.17 no.4
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• pp.36.1-36.6
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• 2019

The incidence and mortality rate of cancer continues to gradually increase, although considerable research effort has been directed at elucidating the molecular mechanisms underlying biomarkers responsible for tumorigenesis. Accumulated evidence indicates that the long non-coding RNAs (lncRNAs), which are transcribed but not translated into functional proteins, contribute to cancer development. Recently, linc00152 (an lncRNA) was identified as a potent oncogene in various cancer types, and shown to be involved in cancer cell proliferation, invasiveness, and motility by sponging tumor-suppressive microRNAs acting as a competing endogenous RNA, binding to gene promoters acting as a transcriptional regulator, and binding to functional proteins. In this review, we focus on the oncogenic role of linc00152 in tumorigenesis and provided an overview of recent clinical studies on the effects of linc00152 expression in human cancers.

• YAKHAK HOEJI
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• v.36 no.6
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• pp.529-537
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• 1992

To investigate the effect of ursolic acid on the expression of oncogenes in tumor cells of mice, sarcoma 180 ascites tumor cells were implanted into the left groin of ICR mice and the tumor bearing mice were treated with ursolic acid. The expression of oncogenes were measured by in situ hybridization method. Ursolic acid significantly reduced the expression of oncogenes in the tumor cells. Therefore, it can be said that the prestated anticarcinogenic effect of ursolic acid could be partly ascribed to the mechanism included in the oncogene´s transcription level.