• International Journal of Industrial Entomology and Biomaterials
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• v.1 no.1
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• pp.53-58
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• 2000

A cDNA encoding the luciferase of firefly Luciola lateralis was cloned downstream from the polyhedrin gene promoter of Bombyx mori nucleopolyhedrovirus and expressed in B. mori cells (BmN-4). The coding soquence for luciferase was inserted into pBmKSK2 rectors) which was reconstructed from the polyhedrin-based transfer vector pBmKSKl by modifying cloning sites. Recombinant virus, BmK2-LUCDF, containing the luciferase gene was selected and purified in BmN-4 cells. The emission of luminescence by luciferase was only detected in BmK2-LUCDF-infected cell extracts. This result indicates that the cloned new luciferase gene of firefly L. lateralis can be expressed efficiently in baculovirus expression system and used as a useful reporter gene.

• Journal of Korean Neurosurgical Society
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• v.46 no.4
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• pp.385-388
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• 2009

Objective : We analyzed the methylation status of the O6-methylguanine-DNA methyltransferase (MGMT) gene promoter in World Health Organization (WHO) grade III gliomas in association with other molecular markers to evaluate their prevalence. Methods : The samples of a total of 36 newly WHO grade III glioma patients including 19 anaplastic oligodendrogliomas (AO), 7 anaplastic oligoastrocytomas (AOA), and 10 anaplastic astrocytomas (AA) were analyzed. The methylation status of the MGMT gene promoter was confirmed by methylation-specific polymerase chain reaction. The 1p/19q chromosomal deletion status and EGFR amplification were assessed by Fluorescence In-Situ Hybridization. MGMT, EGFR, EGFRvlll, and p53 expression were analyzed by immunohistochemical staining. Results : The MGMT gene promoter was methylated in 32 (88.9%) and unmethylated in 4 (11.2%) Among them, all of the AO and AOA had methylated MGMT gene promoter without exception. Significant associations between MGMT gene promoter hypermethylation and 1p/19q deletion was observed (p=0.003). Other molecular markers failed to show significant associations between MGMT gene promoter statuses. Conclusion : There was extensive epigenetic silencing of MGMT gene in high grade gliomas with oligodendroglial component. Together with frequent 1p/19q co-deletion in oligodendroglial tumors, this may add plausible explanations supporting the relative favorable prognosis in oligodendroglial tumors compared with pure astrocytic tumors.

• Animal cells and systems
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• v.4 no.2
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• pp.181-186
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• 2000

The expression of $p21^{WAF1/ClP1/SDl1}$, one of the cyclin-dependent kinase inhibitors, is regulated by a variety of transcription factors including p53 and STAT. Heat shock induces the expression of p21 in a temperature- and time-dependent manner. Although the p21 induction by heat shock has been reported to be controlled by p53, a p53-independent mechanism Is also involved. To understand the p53-independent regulation of heat shock-induced p21 expression, we searched the promoter region of p21 gene and found one or two heat shock element (HSE)-like sequences in human, rat, and mouse. Electromobility shift assay (EMSA) showed that heat shock factor (HSF) could bind to these HSE-like sequences In response to heat shock, even though to a lesser extent than to HSE. In addition, p21 promoter deletion analysis revealed that heat shock activated a p21 deletion promoter construct containing the HSE-like sequences but lacking p53-binding sites, but not a promoter construct containing neither HSE-like sequences nor the p53-responsive element. Furthermore, the p21 induction by heat shook was significantly inhibited in confluent cells in which heat shock-induced HSF activation was reduced. These results suggest that the transcriptional regulation of p21 by heat shock may be mediated through activation and binding to HSE-like sequences of HSF.

• The Journal of the Korean bone and joint tumor society
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• v.20 no.2
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• pp.99-103
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• 2014

Li-Fraumeni syndrome (LFS) is an autosomal dominant hereditary disorder characterised by a variety of different tumor types in children and young adults. That contains with a germline mutation in the tumor suppressor gene Tumor Protein p53 (TP53). That is extremely rare. Furthermore, this is sometimes overlooked. Here, we report a case of LFS which was confirmed by mutational analysis of the p53 gene. Also, literature review is intended to improve understanding of this disease entity.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.33 no.3
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• pp.191-198
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• 2007

The p53 which is well known as tumor suppressor gene is located at 17p13. p53 is a sequence-specific DNA binding transcription factor that responds to certain cytotoxic stresses, such as DNA damage, by enhancing the transcription of genes that regulate cell-cycle progression as well as programmed cell death. The p63 gene that is located at 3q27-29, is recognized members of the p53 family, and responsible for the transcription of 6 isoforms. Three isoforms ($TAp63{\alpha}$, $TAp63{\beta}$, $TAp63{\gamma}$) contain an N-terminal transactivation (TA) domain and can induce apoptosis. The other 3 isoforms (${\Delta}Np63{\alpha}$, ${\Delta}Np63{\beta}$, ${\Delta}Np63{\gamma}$) lack the TA domain and may function in a dominant-negative fashion by inhibiting the transactivation functions of p53 and TAp63 proteins, and thus act as oncoproteins. A number of studies have investigated the role of p63 in human squamous cell carcinomas from different organs. Only a few studies have examined ${\Delta}Np63$ isoform in oral squamous cell carcinoma including normal epithelium. This study aimed to evaluate expression of ${\Delta}Np63$ isoform in human oral squamous cell carcinoma tissue and normal mucosa. The 3 cases of well differenciated oral squamous cell carcinoma specimen including adjacent normal mucosa were examined, and immunohistochemical study with monoclonal antibody(4A4) and tumor cell apoptosis analysis with Transmission Electon Microscopy were studied. And, RT-PCR analysis was done for expression of ${\Delta}Np63$ isoform. The results were as followed. 1. Normal gingiva showed the restricted p63 expression in basal cell layer. 2. Well differentiated squamous cell carcinoma showed mainly p63 expression in overall area of malignancy, especially in basal cell layer to adjacent stromal tissue. 3. Tumor cells around keratinized area with no p63 expression disclosed less micro-organelle in decreased size cytoplasm and severe chromatin margination with nuclear destruction that means apoptosis. 4. Comparison of mRNA expression of ${\Delta}Np63$ isoform by RT-PCR showed variable expression of ${\Delta}Np63$ isoform, but ${\Delta}Np63{\alpha}$ was most highly expressed in all 3 tumor specimen. From theses results, it should be suggested that ${\Delta}Np63$ isoform expression in well differentiated squamous cell carcinoma was closely related to tumor oncogenesis, expecially overexpression of ${\Delta}Np63{\alpha}$ is a most important factor in tumor genesis of oral squamous cell carcinoma.

• Journal of Convergence for Information Technology
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• v.10 no.5
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• pp.134-142
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• 2020

This study aimed to determine whether there was a difference in lung functions of smokers according to the presence of carcinogenic genetic-metabolizing enzymes by comparing the results of lung functions and the presence of genetic metabolizing enzymes that metabolize tobacco substances. To achieve this, 31 smokers without no illness and no psychiatric history were selected (28 males and 3 females); they were aged 20 to 27 years and were physically and mentally healthy students attending K University. Their lung functions were measured, and gene polymorphisms of cytochrome P-450 1A1 (CYP1A1) related to metabolic activation of tobacco components and gene polymorphism of tumor protein 53 (TP53) related to lung cancer were analyzed. As a result, the mean values of lung function of TT and Arg / Arg without genetic mutations were the highest, and ANOVA analysis of CYP1A1 and lung functions showed that the P-value of FVC was 0.049, which was different between groups. In other words, there is no high mutation in Cytochrome P-450 1A1 (CYP1A1) gene, which is associated with the metabolic activation of tobacco components. In other words, In the absence of the mutant Cytochrome P-450 1A1 (CYP1A1) gene, which is associated with the metabolic activation of tobacco components, the value of FVC was high.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.6
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• pp.2917-2922
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• 2014

Background: The p53-binding protein 1 (TP53BP1) gene may be involved in the development of cancer through disrupting DNA repair. However, investigation of associations between TP53BP1 rs2602141 A/C polymorphism and cancer have yielded contradictory and inconclusive outcomes. We therefore performed a meta-analysis to evaluate the association between the TP53BP1 rs2602141 A/C polymorphism and cancer susceptibility. Materials and Methods: Published literature from PubMed, Medline, the Cochrane Library, EMbase, Web of Science, Google (scholar), CBMDisc, Chongqing VIP database, and CNKI database were retrieved. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using fixed or random-effects models. Publication bias was estimated using funnel plots, Begg's and Egger's test. Results: A total of seven studies (3,018 cases and 5,548 controls) were included in the meta-analysis. Our results showed that the genotype distribution of TP53BP1 rs2602141 A/C was not associated with cancer risk overall. However, on subgroup analysis, we found that TP53BP1 rs2602141 A/C was associated with cancer risk within an allele model (A vs C, OR=1.14, 95%CI: 1.01-1.29) and a codominant model (AA vs CC, OR=1.36, 95%CI: 1.06-1.74) in Asians rather than in Caucasians. Subgroup analysis by cancer type, genotype, and with or without adjustment for controls showed no significant association. Conclusions: The findings suggested an association between rs2602141 A/C polymorphism in TP53BP1 gene and increased risk of cancer in Asians.

• BMB Reports
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• v.41 no.2
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• pp.164-169
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• 2008

The tumor suppressor gene p53 regulates apoptotic cell death and the cell cycle. In this study, we investigated the role of p53 in nitric oxide (NO)-induced apoptosis in vascular smooth muscle cells (VSMCs). We found that the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) increased apoptotic cell death in p53-deficient VSMCs compared with wild-type cells. The heme oxygen-ase (HO) inhibitor tin protoporphyrin IX reduced the resistance of wild-type VSMCs to SNAP-induced cell death. SNAP promoted HO-1 expression in both cell types. HO-2 protein was increased only in wild-type VSMCs following SNAP treatment; however, similar levels of HO-2 mRNA were detected in both cell types. SNAP significantly increased the levels of non-heme-iron and dinitrosyl iron-sulfur clusters in wild-type VSMCs compared with p53-deficient VSMCs. Moreover, pretreatment with FeSO4 and the carbon monoxide donor CORM-2, but not biliverdin, significantly protected p53-deficient cells from SNAP-induced cell death compared with normal cells. These results suggest that wild-type VSMCs are more resistant to NO-mediated apoptosis than p53-deficient VSMCs through p53-dependent up-regulation of HO-2.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.1
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• pp.347-350
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• 2012

TP53 is the mostly commonly mutated gene in many cancers and the P53 tumor suppressor protein is involved in multiple cellular processes, including transcription, DNA repair, genomic stability, senescence, cell cycle control and apoptosis. A common single nucleotide polymorphism located within the proline rich region of TP53 gene at codon 72 in exon 4 encodes either proline or arginine. TP53 Arg 72 is more active than TP53 Pro 72 in inducing apoptosis. The aim of this study was to understand the association of the 72 codon polymorphism with acute leukemia development and prognosis. A total of 288 acute leukemia cases comprising 147 acute lymphocytic leukemia (ALL) and 141 acute myeloid leukemia (AML), as well as 245 controls were recruited for analysis of the TP53 72 polymorphism using PCR-RFLP method. Significant association of homozygous arginine genotype with AML was observed (${\chi}^2$- 133.53; df-2, p < 0.001. When data were analyzed with respect to clinical variables, elevation in mean WBC, blast %, LDH levels and slight reduction in DFS in ALL cases with the arginine genotype was observed. In contrast, AML patients with Pro/Pro had elevated WBC, Blast%, LDH levels with slightly reduced DFS. Our study indicates that Arg/Arg genotype might confer increased risk to development of acute myeloid leukemia.

• Molecules and Cells
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• v.42 no.11
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• pp.773-782
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• 2019

Cellular senescence is an irreversible form of cell cycle arrest. Senescent cells have a unique gene expression profile that is frequently accompanied by senescence-associated heterochromatic foci (SAHFs). Protein kinase CK2 (CK2) downregulation can induce trimethylation of histone H3 Lys 9 (H3K9me3) and SAHFs formation by activating SUV39h1. Here, we present evidence that the PI3K-AKT-mTOR-reactive oxygen species-p53 pathway is necessary for CK2 downregulation-mediated H3K9me3 and SAHFs formation. CK2 downregulation promotes SUV39h1 stability by inhibiting its proteasomal degradation in a p53-dependent manner. Moreover, the dephosphorylation status of Ser 392 on p53, a possible CK2 target site, enhances the nuclear import and subsequent stabilization of SUV39h1 by inhibiting the interactions between p53, MDM2, and SUV39h1. Furthermore, $p21^{Cip1/WAF1}$ is required for CK2 downregulation-mediated H3K9me3, and dephosphorylation of Ser 392 on p53 is important for efficient transcription of $p21^{Cip1/WAF}$. Taken together, these results suggest that CK2 downregulation induces dephosphorylation of Ser 392 on p53, which subsequently increases the stability of SUV39h1 and the expression of $p21^{Cip1/WAF1}$, leading to H3K9me3 and SAHFs formation.