Li L.,University of Sichuan |
Wu J.,Chongqing Cancer Hospital |
Sima X.,University of Sichuan |
Bai P.,University of Sichuan |
And 7 more authors.
Tumor Biology | Year: 2013
Growing evidence indicates that tumor suppressor gene TP-53 and non-coding RNA miR-34b/c independently and/or jointly play crucial roles in carcinogenesis. We hypothesized that the polymorphisms of rs4938723 in the promoter region of pri-miR-34b/c and TP-53 Arg72-Pro may be related to the risk of nasopharyngeal carcinoma (NPC). We performed a case-control study between 217 patients with NPC and 360 healthy controls in a Chinese population using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. A significantly increased risk of NPC was observed in the miR-34b/c rs4938723 CT/CC genotypes compared with the TT genotype (adjusted OR = 1.44, 95 % CI 1.02-2.03, p = 0.04), and also the C allele (adjusted OR = 1.33, 95 % CI 1.04-1.70, p = 0.03). The gene-gene interaction of miR-34b/c rs4938723 and TP-53 Arg72-Pro showed that the combined genotypes of rs4938723CT/CC and TP-53CG/CC increased the risk of NPC (rs4938723CT/CC + TP-53CG/CC vs. rs4938723 TT + TP-53 CG/CC: OR = 1.58, 95 % CI 1.04-2.42, p = 0.03). These findings suggest that miR-34b/c rs4938723 and TP-53 Arg72Pro polymorphisms may singly or collaboratively contribute to the risk of NPC. © 2013 International Society of Oncology and BioMarkers (ISOBM).
Yu W.,Kunming General Hospital of Chengdu Military Command |
Li G.,Third Military Medical University |
Wang D.,Chongqing Cancer Hospital
Chinese Journal of Clinical Oncology | Year: 2014
Objective: To observe the effect of the proteininhibitor of activated STAT 3 (PIAS3) on the proliferation and apoptosis of U251 glioma cells after PIAS3 expression was inhibited by RNAi. Methods: Three RNAi expression vectorstargeting PIAS3 were constructed and transfected into CHG-5 cells by liposomein vitro. The most efficient RNAi vector was subsequently selected by examiningthe mRNA expressions of PIAS3 in the transfected cells by semi-quantitativeRT-PCR. The selected RNAi vector was then transfected into U251 cells. After 48h of transfection, the mRNA and protein expressions of PIAS3 in glioma cellswere examined by semi-quantitative RT-PCR and western blot. Apoptosis wasobserved by flow cytometry using a double-staining method with FITC-conjugatedannexin V and PL Flow cytometry was also applied in cell cycle assay. Results: RNAidownregulated the mRNA (P<0.01) and protein (P<0.01) expressionsof PIAS3 in transfected cells.RNAi promoted the resistance of U251 cells to apoptosisand subsequently altered the cell cycle. A high percentage of G2 phaseand a low percentage of Sphase were observed in U251 cells. Conclusion: The downregulation of PIAS3arrested U251 cells in the G2 phase andinduced the resistance of U251 cells to apoptosis.
Ji H.,Kunming General Hospital of Chengdu Military Command |
Yu W.,Kunming General Hospital of Chengdu Military Command |
Li G.-H.,Chongqing Medical University |
Wang D.-L.,Chongqing Cancer Hospital |
Chen H.,Kunming General Hospital of Chengdu Military Command
Chinese Journal of Cancer Prevention and Treatment | Year: 2015
OBJECTIVE: To observe the effects of overexpression of protein inhibitor of activated STAT3(PIAS3) on the proliferation and apoptosis in CHG-5 glioma cells. METHODS: The constructed eukaryotic expression vectors of PIAS3 was constructed named as pEGFP-N1-PIAS3. In vitro the CHG-5 glioma cells were transfected with pEGFP-N1-PIAS3 with 01-igofectamine. At the same time, the blank control and negative control groups were set. After 48 hours, the expression of PIAS3 was analyzed by RT-PCR, western blots and immunohistochemistry. The apoptosis and proliferation of the transfected cells were analyzed by flow cytometry. RESULTS: The expression of PIAS3 in the transfected cells was increased. The change of cell shape and increased necrotic cells were observed by microscope. The IDV (Integrated density value) of PIAS3 mRNA (523 414.5±34 502.89) in the PIAS3-transfected group was significantly different from that of the blank control group (135 668.0±6 693.66) and the negative control group (154 511.67±8 266.89; χ2 = 13.053, P = 0.01). The IDV of PIAS3 protein (30.13±3.76) in the PIAS3-transfected group was significantly different from that of the blank control group (13.83±0.77) and the negative control group (15.02±0.87; χ2 = 14.193, P = 0.001). The results suggested that the expression of PIAS3 was increased in the PIAS3-transfected cells. The percentage of early apoptotic cells (12.5±1.9)% in the PIAS3-transfected group was significantly higher than that of the blank control group (6.4±1.1)% and the negative control group (5.4±1.8)% (χ2=7.407, P = 0.005). The rate of living cells (86.9±2.2)% was significantly lower than that of the blank control group (92.1±1.2)% and the negative control group (93.1±2.0)% (χ2=4.775, P=0.019). The percentage of the cells in S phase (35.2±4.2)% in the PIAS3-transfected group was significantly higher than that of the blank control group (24.5±5.1)% and the negative control group (23.0±3.7)%(χ2 = 8.179, P=0.003). The percentage of the cells in G2 phase (10.7±5.4)% in the PIAS3-transfected group was significantly lower than that of the blank control group (21.3±4.0)% and the negative control group (27.8±5.2)% (χ2 = 17.121, P<0.01). CONCLUSION: The overexpression of PIAS3 in CHG-5 glioma cells significantly suppresses cells proliferation, induces S-phase arrest and cell apoptosis. © 2015, Editorial Board of Chinese Journal of Cancer Prevention and Treatment. All right reserved.
Yang D.,Chongqing Cancer Hospital |
Zou X.,Chongqing University |
Yi R.,Chongqing University |
Liu W.,Chongqing Medical University |
Zhao X.,Chongqing University
Applied Biological Chemistry | Year: 2016
This study was conducted to investigate the in vitro anticancer reinforcing effects of neferine (Nef) on dehydroepiandrosterone (DHEA) and the mechanism was also determined during the investigation. By the growth effects of Nef and DHEA on MCF-7 human breast cancer cells, 8 mg/mL Nef was a non-virulent concentration in MCF-7 cells, and this concentration was used for further experiment. In 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide assay, 30 mg/mL DHEA showed 49.4 % growth inhibitory effect in MCF-7 cells, whereas Nef (8 mg/mL) + DHEA (30 mg/mL) treatment had the higher effect at 67.8 %. The flow cytometry analysis results showed that 15 and 30 mg/mL DHEA-treated MCF-7 cells had 12.2 and 21.6 % apoptotic cells, respectively, Nef + DHEA could raise the apoptotic cells to 36.7 %. Reverse transcription-polymerase chain reaction assay shows remarkable results according to which DHEA could significantly increase caspase-3, caspase-8, caspase-9, Bax, p53, p21, E2F1, Fas, FasL mRNA expressions and decrease Bcl-2, Bcl-xL, HIAP-1, HIAP-2, survivin expressions as compared to the untreated control cancer cells. Moreover, these effects depend on the concentration of DHEA, and Nef which could further strengthen these effects. From these results, low concentration of Nef could not influence the growth of MCF-7 cells, but using its sensitization effect, Nef raised the in vitro effects of DHEA. Nef could be got easily. With these results we can accomplish that Nef + DHEA might be used as the new anticancer materials combination. © 2016, The Korean Society for Applied Biological Chemistry.
Wu H.-T.,Zunyi Medical College |
Ruan J.,Chongqing Cancer Hospital |
Zhang X.-D.,Chongqing Medical University |
Xia H.-J.,Chongqing Medical University |
And 2 more authors.
Brain Research | Year: 2010
Cerebral vasospasm (CV) is the main complication of spontaneous subarachnoid hemorrhage (SAH), affecting clinical outcome of patients with SAH. Accumulating evidence indicates that apolipoprotein E (apoE protein, APOE gene) gene polymorphism is associated with prognosis of patients with SAH. The current study aimed to investigate the association of promoter polymorphism of APOE with CV in patients with SAH. One hundred and one patients with spontaneous SAH were involved in this study. Venous blood samples were collected to identify the promoter genotype of APOE by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). CV was judged by transcranial Doppler sonography (TCD) combined with patients' condition. Associations of APOE promoter polymorphism with CV after SAH were analyzed by χ2 test, uni- and multivariate logistic regression analyses. In 101 patients, 42 of 87 patients (48.3%) with promoter - 219T allele showed CV, which was significantly different from those with - 219G allele (23/61, 37.7%, P = 0.04). Uni- and multivariate logistic regression analyses also showed that promoter - 219T was a risk factor to predispose CV after SAH. However, there was no significant association between promoter - 491A/T (rs#449647) or - 427C/T (rs#769446) polymorphisms and SAH induced CV (P > 0.05). Our finding suggests that patients with APOE - 219T promoter are apt to CV after spontaneous SAH. © 2010 Elsevier B.V. All rights reserved.