Salari Fanoodi, T. (2015) P21 tumor suppressor gene expression evaluation in esophagus cancer patients. Masters thesis, University of Zabol.
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Abstract
Background and objectives: Cancer is the third most common cause of death in Iran and 30,000 Iranians lose their lives each year due to cancer. Esophageal cancer is the eighth most common cancer and the sixth cause of cancer death worldwide and is reported to include more than 80% of all death cases in developing countries. P21 protein is encoded by WAF1/CIP1, a tumor suppressor gene located on chromosome 2.6P21. This protein is known as one of the proteins related to cell cycle; P21 stimulation is a common mechanism of growth inhibition in different physiological conditions. Materials and methods: The present case-control study randomly selected15 paraffin-embedded esophageal cancer tissue and 15 paraffin-embedded normal esophageal samples, collected from different medical centers of Zahedan and Kashan. RT-qPCR reactions were performed with three repetitions for P21 gene and internal control (GAPDH) by Livac method 2-ΔΔCT for all samples and was analyzed using SPSS software. Results: The results indicated no significant difference in P21 gene expression between patients and controls (p>0.05). Also, no significant difference was observed in P21 gene expression between males and females (p>0.05). Discussion: No significant differences were observed in P21 gene expression. P21 protein exists in low amount in most cells being reproduced. As protein P53 is activated by DNA fractures or intermediate replicators, it is connected to motifs in promoter CDKN1A (the gene coding P21 protein) and increases transcription of CDKN1A gene sharply. But the transcriptions of CDKN1A gene are impaired in cancer cells, produced during P53 mutations and thus fail to limit the progression of cell cycle in response to DNA damage and the incomplete cloned chromosome. The intracellular levels of this protein increases in cancerous tissue due to P53 gene mutations and increased half-life of the mutant form of the protein, but can’t express P21 gene due to lack of normal function. Regarding the activation pathways of P21 (dependentonP53 and independent of P53), increase in the expression of P53, D-cycline, MYC, and Ras causes lack or reduction in P21 expression. Biological and network adjustment activity of P21 complex makes predictions about its function to make cancer treatment possible. No relationship between the expression of P21WAF1 and clinical pathologic parameters was found regarding sex and age (Liu et al., 2006)
| Item Type: | Thesis (Masters) |
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| Uncontrolled Keywords: | Esophageal cancer, paraffin-embedded tissue, gene expression, P21 gene, RT- qPCR |
| Subjects: | Q Science > QH Natural history > QH301 Biology |
| Depositing User: | admin admin1 admin2 |
| Date Deposited: | 01 Nov 2016 07:34 |
| Last Modified: | 01 Nov 2016 07:34 |
| URI: | http://eprints.uoz.ac.ir/id/eprint/951 |
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