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Objective:This work aims to detect the levels of miR-200c/141 methylation and miR-200c/141 in gastric cancer tissue and investigate the relationship between miR-200c/141 expression and clinical parameters. Methods:The methylation status of miR-200c/141 CpG island and miR-200c/141 in gastric cancer tissue specimens was evaluated by qRT-PCR or BS-MSP method. We analyzed the relationship among the methylation status of miR-200c/141 CpG island, expression level of miR-200c or miR-141, and clinical parame-ters. Results:The status of miR-200c/141 CpG island methylation in gastric cancer tissue was significantly higher compared with that in paracarcinoma tissue. MiR-200c and miR-141 were markedly decreased in gastric cancer tissue compared with those in adjacent tis-sue. MiR-200c/141 CpG island methylation was negatively related with the expression of miR-200c and miR-141 in gastric cancer speci-mens. Conclusion:The upregulation of miR-200c/141 CpG methylation inhibits miR-200c/141 expression in gastric cancer tissue.
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As a tumor-specific antigen highly expressed in various types of tumors, MACE-A does not exist in normal adult tissues, except for testis and placenta. Therefore MAGE-A antigens are regarded. tumor specific antigen,and have significant significance for cancer immunotherapy.
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Background and purpose: Protein kinase P1k3 could increase the transcriptional activity of p53. However, the effect of P1k3 on the transcriptional activity of p73 is still unknown. Our study was to investigate the effect of P1k3 on the transcriptional activity of p73. Methods: Luciferase reporter assay, RT-PCR and colony formation assay were adopted to study the effect of P1k3 and kinase-deficient P1k3 (K52R) on the transcriptional activity of p73 in p53-deficient human lung carcinoma H1299 cells. Results: Luciferase reporter assay showed that p73 increased the luciferase activities induced by p21~(WAF1) and Bax promoters (P<0.05). After co-transfection with p73 and P1k3, the luciferase activities induced by p21~(WAF1) and Bax promotors were significantly decreased in a dose-dependent manner as compared with the group that transfected p73 only (P<0.05). However, kinase-deficient Plk3 (K52R) had no significant effect on the luciferase activities induced by p21~(WAF1) and Bax promoters (P>0.05). RT-PCR showed that p73 increased the mRNA expressions of p21~(WAF1) and BAX (P<0.05). P1k3 decreased the expressions of p21~(WAF1) and Bax induced by p73 (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the expressions of p21~(WAF1) and Bax induced by p73 (P>0.05). Colony formation assay revealed that p73 decreased the colony formation of H1299 cells (P<0.05). P1k3 decreased the inhibitory effect of p73 on the colony formation of H1299 cells (P<0.05). Kinase-deficient P1k3 (K52R) had no significant effect on the inhibitory effect of p73 on the colony formation of H1299 cells (P>0.05).Conclusion: P1k3 can inhibit the transcriptional activity of p73, where as kinase-deficient P1k3 has no effect on the transcriptional activity of p73.
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Objective:To study the correlation of C(-938)A single nucleotide polymorphism (SNP) in the promoter of anti-apoptosis gene Bcl-2 with the clinical biological parameters of breast cancer patients in Hebei Province. Methods:Three genotypes(AA, AC, CC) of Bcl-2 C(-938)A from 113 samples of breast cancer patients were analyzed by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, and the results were associated with clinical biological parameters. The distribution of genotype frequency was compared between different groups. Results:When stratified for axillary lymph node metastases, the frequency of AA genotype were 26.8%, 47.8% and 52.6% and the distribution of AC+CC genotypes were 73.2%, 52.2% and 47.4% in negative group, 1-3 metastasis group, and ≥4 metastasis group. The difference between the two groups was significant (χ~2=6.337, P=0.042). Compared with the AC+CC genotypes, the OR value of AA genotype in ≥4 metastasis group was 3.041 (95%CI=1.072-8.626). The frequency of AA genotype were 30.9% and 69.1% in gradeⅠ-Ⅱ group and grade Ⅲ group, and the frequency of AC+CC genotypes were 57.9% and 42.1%. The difference between the two groups was significant (χ~2=5.055; P=0.025). Compared with the AC+CC genotypes, the OR value of AA genotype in differentiated tumors(grade Ⅲ)was 3.082 (95%CI=1.122-8.465). Stratified for estrogen receptor (ER), progesterone receptor (PR) and C-erbB2, there was no difference between the distribution of AA genotype and AC+CC genotypes (χ~2=3.005, χ~2=1.504, χ~2=1.163, P>0.05). Conclusion:The AA genotype of Bcl-2 gene C(-938)A maybe correlated with high lymph node metastasis rate and poor differentiation.