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Xiaojuan Z.,Xian Jiaotong University | Xiaomin S.,Xian Jiaotong University | Yunmei W.,Cancer Hospital of Shaanxi Province | Jianjian L.,Xian Jiaotong University
Chinese Journal of Cancer Biotherapy | Year: 2013

Objective:To investigate the inhibitoty effects of recombinant adenovirus-p53 (rAd-p5J) on the growth of lung adenocarcinoma H1299 cells (wtP53-/-) in vitro and in vivo, and observe the treatment feasibility of lung adenocarcinoma with tail intravenous injection of rAd-p53. Methods: MTT assay was performed to detect the inhibitory effect of rAd-p53 on the proliferation of H1299 cells. After transfected by rAd-p53 with multiplicity of infection (MOI) =500, the expression of p53 mRNA in H1299 cells was detected by RT-PCR at 24 h; the expression of P53 protein in H1299 cells and the apoptosis of H1299 cells were detected at 72 h by Western blotting and flow cytometry, respectively. BALB/c nude mice were injected subcutaneously with H1299 cells to establish a lung adenocarcinoma nude mice model and then the mice were intravenously administrated by rAd-p53; the tumor growth was observed and tumor growth curve was drawn. Results: H1299 cells were infected by rAd-p5J with MOI =500; after infection for 24 h, wild-type p53 mRNA was expressed in rAd-p53 group, and at 72 h, wt P53 protein was detected in rAd-p53 group. rAd-p53 infection could significantly inhibit the proliferation of H1299 cells, the cell proliferation ratio of rAd-p53 group was significant lower than that of the control group (2. 8 ± 0. 4 vs 6. 1 ± 0. 5, P < 0. 05). The apoptotic rates of H1299 cells in rAd-p5J group were in-creased with time, which were significantly higher than those in the control group ({divides}27.6±0.05j% to{divides}4.9±0.09J%, P <0.01) after infection for 48 h. H1299 tumor-bearing nude mice were successfully established, and the tumor volume of rAd-p53 group was significantly smaller than that of the control group even two weeks after tail intravenous injection ([0. 875 ±0. 253] cm3 vs [0. 479 ± 0. 215] cm3,P < 0. 05). Conclusion: Tail intravenous infection of rAd-p53 could up-regulate the protein expression of P53 in H1299 cells, then restrain the growth of H1299 cells, promote the apoptosis and significantly inhibit the growth of H1299 cell xenograft tumors in nude mice. Source


Dai Z.-J.,The Second Affiliated Hospital Of Xian Jiaotong University | Dai Z.-J.,University of Science and Technology of China | Shao Y.-P.,University of Science and Technology of China | Wang X.-J.,The Second Affiliated Hospital Of Xian Jiaotong University | And 7 more authors.
Current Pharmaceutical Design | Year: 2015

Objectives: To evaluate the relationship between the five common polymorphisms in miRNAs (miR-146a rs2910164 G>C, miR-149 rs2292832 C>T, miR-196a2 rs11614913 C>T, miR-499 rs3746444 A>G and miR-27a rs895819 A>G), and breast cancer (BC) risk. Methods: Meta-analyses were performed on 15 published studies involving 8, 361 BC patients and 8, 504 cancer-free controls. There were 8 studies with 4, 314 cases and 4, 485 controls for rs2910164, 3 studies with 1, 439 cases and 1, 508 controls for rs2292832, 10 studies with 4, 618 cases and 5, 590 controls for rs11614913, 5 studies with 2, 924 cases and 3, 563 controls for rs3746444, and 5 studies with 2, 912 cases and 3, 697 controls for rs895819. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the BC risk. Results: Meta-analyses showed that rs2910164 (miR-146a) was associated with BC risk in Caucasian population (homozygote comparison: OR = 1.29, 95%CI = 1.02-1.63, P=0.03; dominant model: OR = 1.31, 95% CI = 1.05-1.65, P=0.02), whereas negative results were obtained for Asians in all genetic models. rs11614913 (miR-196a2) was associated with BC risk in the overall population based on the recessive model (OR = 0.89, 95% CI = 0.80-0.99, P=0.03). Association of rs3746444 (miR-499) with BC risk was detected under three genetic models (allele contrast genetic model: OR = 1.13, 95%CI = 1.03-1.23, P=0.007; homozygote comparison: OR = 1.36, 95%CI = 1.10-1.69, P=0.005 and recessive model: OR = 1.38, 95% CI = 1.12-1.70, P=0.003). When stratified by ethnicity, the effects remained in Asians. rs895819 (miR-27a) was associated with BC risk in the overall population based on the allele contrast genetic model (OR = 0.91, 95%CI = 0.85-0.98, P=0.02); heterozygote comparison (OR = 0.89, 95%CI = 0.80-0.99, P=0.03) and the dominant model (OR = 0.89, 95% CI = 0.80-0.98, P=0.02). However, there was no association between rs2292832 (miR-149) polymorphism and BC susceptibility. Conclusion: Our meta-analysis results suggested that the rs2910164 and rs3746444 polymorphisms are associated with increased BC risk, while the rs11614913 and rs895819 polymorphisms correlate with reduced BC risk. © 2015 Bentham Science Publishers Source


Wang G.,Xian Jiaotong University | Lei L.,Cancer Hospital of Shaanxi Province | Zhao X.,Cancer Hospital of Shaanxi Province | Zhang J.,Cancer Hospital of Shaanxi Province | And 2 more authors.
Oncology Research | Year: 2015

Calcitriol (1a,25-dihydroxyvitamin D3) has demonstrated anticancer activity against several tumors. However, the underlying mechanism for this activity is not yet fully understood. Our experiment was designed and performed to address one aspect of this issue in cervical cancer. HeLa S3 cells were cultured in media with various concentrations of calcitriol. Cell proliferation and cell cycle were assessed by spectrophotometry and flow cytometry, respectively. The mRNA and protein expression levels of human cervical cancer oncogene (HCCR-1) and p21 were determined by RT-PCR and Western blot, respectively. Results indicated that calcitriol inhibited HeLa S3 cell proliferation and induced cell cycle arrest at the G1 phase. Calcitriol decreased HCCR-1 protein expression in a dose- and time-dependent manner. Furthermore, promoter activity analyses revealed that transcriptional regulation was involved in the inhibition of HCCR-1 expression. Overexpression of HCCR-1 in HeLa S3 cells reversed the inhibition of cell proliferation and G1 phase arrest that resulted from calcitriol treatment. In addition, calcitriol increased p21 expression and promoter activity. HCCR-1 overexpression decreased p21 expression and promoter activity. Thus, our results suggested that calcitriol inhibited HeLa S3 cell proliferation by decreasing HCCR-1 expression and increasing p21 expression. Copyright © 2015 Cognizant Comm. Corp. Source

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