Identification of a polymorphic site as a mutational site in exon VI of the mouse p53 gene

Background: The role of p53 gene in the gastric cancer is still controversial. This study is aimed at determining the rate of the p53 gene codon 72 polymorphisms in gastric cancer patients and evaluating the relationship between these polymorphisms and endoscopic and histopathological features of gastric cancer. Patients and methods: Sixty eight patients with gastric cancer (cases) and one hundred and thirty six patients without gastric cancer (controls) were enrolled. p53 gene codon 72 polymorphisms were determined by PCR-RFLP technique with DNA extracted from samples of gastric tissue. Results: In the group of gastric cancer, Arginine/Argnine, Arginine/Proline and Proline/Proline genotypes were found in 29.4%, 42.7% and 27.9%, respectively. The differences of rates were not statistically significant between cases and controls (p > 0,05). In males, the Proline/Proline genotype was found in 38.1% in patients with gastric cancer and more frequent in patients without gastric cancer (15.7%, p = 0,01). An analysis of ROC curve showed that the cut-off was the age of 52 in the Proline/Proline genotype, but it was 65 years old in the Arginine/Proline genotype. The Proline/Proline genotype was found in 41.9% in Borrmann III/IV gastric cancer, this rate was higher than Borrmann I/II gastric cancer (16.2%, p = 0.037) and also higher than controls (18.4%, p = 0,01). The rate of Proline/Proline genotype was 41.7% in the diffuse gastric cancer, it was higher than in controls (p = 0,023). Conclusion: No significative difference of rate was found in genotypes between gastric cancer group and controls. However, there was the relationship between Proline/Proline genotype and gastric cancer in males, Borrmann types of gastric cancer, the diffuse gastric cancer. Key words: polymorphism, codon 72, p53 gene, PCR - RFLP, gastric cancer.

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Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

International Electronic Journal of Medicine ◽

10.34172/iejm.2020.03 ◽

2020 ◽

Vol 9 (1) ◽

pp. 14-20

Author(s):

Mohammad Zamani Rarani ◽

Fahimeh Zamani Rarani ◽

Ali Valiani ◽

Zeinolabedin Shrifian Dastjerdi ◽

Elias Kargar Abargouei ◽

...

Keyword(s):

Cell Line ◽

Cancer Cell Line ◽

P53 Gene ◽

T47d Cell ◽

Adenosine A1 Receptor ◽

T47d Cells ◽

Apoptosis Rate ◽

Adenosine A1 ◽

T47d Cell Line ◽

A1 Receptor

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

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423. The Combination of p53 Dendritic Cell Vaccine and Ad-p53 Gene Therapy Against p53 Overexpressing and p53 Deleted Tumor Cell Lines

Molecular Therapy ◽

10.1016/s1525-0016(16)34032-1 ◽

2015 ◽

Vol 23 ◽

pp. S167

Author(s):

Hiroki Saito ◽

Koichi Kitagawa ◽

Risa Yamasaki ◽

Nami Katai ◽

Naoya Morishita ◽

...

Keyword(s):

Gene Therapy ◽

Dendritic Cell ◽

Tumor Cell ◽

Cell Lines ◽

P53 Gene ◽

Dendritic Cell Vaccine ◽

Cell Vaccine ◽

Tumor Cell Lines

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The status of the p53 gene in human papilloma virus positive or negative cervical carcinoma cell lines

Carcinogenesis ◽

10.1093/carcin/13.7.1273 ◽

1992 ◽

Vol 13 (7) ◽

pp. 1273-1275 ◽

Cited By ~ 26

Author(s):

Shiv Srivastava ◽

Yue A. Tong ◽

Krishnakumar Devadas ◽

Zhi-Qiang Zou ◽

Yawen Chen ◽

...

Keyword(s):

Human Papilloma Virus ◽

Cell Lines ◽

Cervical Carcinoma ◽

Carcinoma Cell ◽

P53 Gene ◽

Papilloma Virus ◽

Carcinoma Cell Lines ◽

The Status

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Targeting Post-Translational Modifications of the p73 Protein: A Promising Therapeutic Strategy for Tumors

Cancers ◽

10.3390/cancers13081916 ◽

2021 ◽

Vol 13 (8) ◽

pp. 1916

Author(s):

Ziad Omran ◽

Mahmood H. Dalhat ◽

Omeima Abdullah ◽

Mohammed Kaleem ◽

Salman Hosawi ◽

...

Keyword(s):

Current Knowledge ◽

Protein A ◽

P53 Gene ◽

Cancer Therapies ◽

Transactivation Domain ◽

P53 Family ◽

Post Translational Modifications ◽

P53 Status ◽

Apoptotic Effects ◽

High Degree

The tumor suppressor p73 is a member of the p53 family and is expressed as different isoforms with opposing properties. The TAp73 isoforms act as tumor suppressors and have pro-apoptotic effects, whereas the ΔNp73 isoforms lack the N-terminus transactivation domain and behave as oncogenes. The TAp73 protein has a high degree of similarity with both p53 function and structure, and it induces the regulation of various genes involved in the cell cycle and apoptosis. Unlike those of the p53 gene, the mutations in the p73 gene are very rare in tumors. Cancer cells have developed several mechanisms to inhibit the activity and/or expression of p73, from the hypermethylation of its promoter to the modulation of the ratio between its pro- and anti-apoptotic isoforms. The p73 protein is also decorated by a panel of post-translational modifications, including phosphorylation, acetylation, ubiquitin proteasomal pathway modifications, and small ubiquitin-related modifier (SUMO)ylation, that regulate its transcriptional activity, subcellular localization, and stability. These modifications orchestrate the multiple anti-proliferative and pro-apoptotic functions of TAp73, thereby offering multiple promising candidates for targeted anti-cancer therapies. In this review, we summarize the current knowledge of the different pathways implicated in the regulation of TAp73 at the post-translational level. This review also highlights the growing importance of targeting the post-translational modifications of TAp73 as a promising antitumor strategy, regardless of p53 status.

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