Letter to the Editor Clarification of data for a meta-analysis: p53 codon 72 polymorphism and prostate cancer risk

Mi, Yuanyuan; Zhu, Lili; You, Xiaoming; Wu, Shan

doi:10.4238/2012.july.19.15

Cited by 2 publications

(1 citation statement)

References 7 publications

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“…Overexpression of p53 is thought to be associated with tumor metastasis, relapse, and poor prognosis. The p53 gene mutation occurs in more than 50% of all malignant tumors (Mi et al, 2012). The protein coded by this gene is a transcription factor that controls initiation of the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

Effect of p53 gene polymorphism on functions of prostate cancer cells

Chi¹,

Yun²,

Tan³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Prostate cancer cells were transfected with plasmids [empty plasmids, wild-type pcDNA3.1-p53 (V/V), mutant type pcDNA3.1-p53 (G/G)] to analyze the effect of p53 gene polymorphisms on the proliferation, cycle, and apoptosis of prostatic cancer cells. Empty plasmids containing wild-type pcDNA3.1-p53 (V/V) and mutant type pcDNA3.1-p53 (G/G) were used to transfect PC3 and LNCaP cells, respectively. Cell proliferation was detected at 0, 24, 48, and 72 h using the MTT method. Cells were collected at 24 and 72 h. The distribution of cell cycles in various groups was detected using flow cytometry (propidium iodide staining method) and the apoptosis rate was detected using annexin V + propidium iodide double staining. Compared with the control group, wild-type pcDNA3.1-p53 (V/V) and mutant type pcDNA3.1-p53 (G/G) showed a significant inhibitory effect on cell proliferation (P < 0.05); the inhibitory effect of the mutant type was stronger than that of the wild-type. There was no significant difference between PC3 cells and LNCaP cells. After transfection with wild-type pcDNA3.1-p53 (V/V) and mutant type pcDNA3

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Section: Discussionmentioning

confidence: 99%

Effect of p53 gene polymorphism on functions of prostate cancer cells

Chi¹,

Yun²,

Tan³

et al. 2015

Genet. Mol. Res.

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MDM2 and P53 polymorphisms contribute together to the risk and survival of prostate cancer

et al. 2015

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The p53 gene and MDM2 gene play critical roles in cell cycle arrest and apoptosis together. Here, we evaluated the associations of prostate cancer risk and survival with the joint effects of mdm2 and p53 polymorphisms. Totally 1,193 cases and 1,310 age frequency-matched controls were included in the study. Prostate cancer patients were followed to determine the intervals of overall survival and disease-free survival. The Pro72Arg Pro allele (homozygous and heterozygous) were significantly associated with prostate cancer risk with an odds ratio (OR) of 0.77 [95% confidence interval(CI), 0.64-0.93]. SNP309 T alleles were associated with a significantly decreased prostate cancer risk among Pro72Arg Pro alleles carriers (OR=0.79, 95% CI, 0.64-0.98). In addition, comparedwith the Pro72Arg Pro alleles and SNP309 G homozygous, patients carrying both SNP309 T alleles and Pro72Arg Arg homozygous had more favorable disease-free survival (hazard ratio [HR] = 0.59, 95% CI, 0.38-0.93). Our results indicated that SNP309 and Pro72Arg polymorphisms may jointly contributeto the etiology and prognosis of prostate cancer.

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Letter to the Editor Clarification of data for a meta-analysis: p53 codon 72 polymorphism and prostate cancer risk

Cited by 2 publications

References 7 publications

Effect of p53 gene polymorphism on functions of prostate cancer cells

Effect of p53 gene polymorphism on functions of prostate cancer cells

MDM2 and P53 polymorphisms contribute together to the risk and survival of prostate cancer

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