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1.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-931674

RESUMO

Objective:To detect the expression of MYBL2 gene in gastric adenocarcinoma tissue and its effects on cell proliferation and invasion. Methods:A total of 100 cases of gastric adenocarcinoma tissue and 100 cases of paracancerous tissue were selected from patients who received surgery in The People's Hospital of Yuhuan between January 2017 and December 2020. Gastric adenocarcinoma cell lines MGC-803 were transfected with MYBL2 siRNA and siRNA control. The cells not transfected were used as controls. MYBL2 gene expression in gastric adenocarcinoma tissue and paracancerous tissue as well as MGC-803 were determined by quantitative real time-polymerase chain reaction. MGC-803 cell proliferation was determined by MTT. The invasive ability of MGC-803 cells was determined by Transwell assay. The migration ability of MGC-803 cells was determined by Scratch testing. MYBL2 protein expression in gastric adenocarcinoma tissue and paracancerous tissue as well as MGC-803 cells was determined by western blotting. Results:The relative mRNA expression of MYBL2 in gastric adenocarcinoma tissue was significantly higher than that in paracancerous tissue [(0.65 ± 0.17) vs. (0.18 ± 0.05), t = 26.52, P < 0.05). The relative mRNA expression of MYBL2 in the MYBL2 siRNA group (0.29 ± 0.07) was significantly lower than that in the control group (0.73 ± 0.12) and siRNA group (0.71 ± 0.16, t = 5.48, 4.16, both P < 0.05). MTT assay showed that after 24 and 48 hours of culture, MGC-803 cell proliferation rate in the MYBL2 siRNA group [(40.95 ± 5.46)%, (52.12 ± 12.27)%] was significantly lower than that in the control group [(67.84 ± 6.45)%, (87.83 ± 9.96)%] and siRNA group [(66.98 ± 7.85)%, (85.98 ± 10.24)%, t = 5.51, 3.91, 4.71, 3.67, all P < 0.05]. MGC-803 cell invasion rate in the MYBL2 siRNA group [ (62.12 ± 6.43)%] was significantly lower than that in the control group [(89.74 ± 6.56)%] and siRNA group [(88.83 ± 7.85)%, t = 5.20, 4.55, both P < 0.05]. The number of MGC-803 cells migrated in the MYBL2 siRNA group [(4.32 ± 0.84) × 10 3] was significantly lower than that in the control group [(8.95 ± 1.64) × 10 3] and siRNA group [(8.83 ± 1.78) × 10 3, t = 4.35, 3.96, both P < 0.05]. The gray value of MYBL2 protein in the gastric adenocarcinoma tissue was (0.56 ± 0.15), which was significantly higher than that in the paracancerous tissue [(0.23 ± 0.07), t = 19.93, P < 0.001]. The gray value of MYBL2 protein in the MYBL2 siRNA group was (0.21 ± 0.03), which was significantly lower than that in the control group (0.67 ± 0.15) and siRNA group (0.65 ± 0.19) ( t = 5.20, 3.96, both P < 0.05). Conclusion:MYBL2 gene is highly expressed in gastric adenocarcinoma tissue. siRNA silencing MYBL2 can decrease the ability of MGC-803 cells to proliferate, invade and migrate and downregulate MYBL2 expression. This study is highly innovative and scientific.

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-513094

RESUMO

Objective To observe the correlation between CD4+ CD29+ T cells and metastasis and radiotherapy for patients with pulmonary adenocarcinoma. Method Seventy-one patients with lung adenocarcinoma, 93 patients with lung adenocarcinoma ,76 cases of chronic obstructive pulmonary disease (COPD),63 cases of healthy volunteers were enrolled. Frequencies of blood CD4+ CD29+ T cells and their intracellular necrosis factor alpha(TNF-α)and interleukin 1(IL-1)were compared. Compare TNF-α,IL-1,integrin beta 1 and vascular endothelial growth factor(VEGF)levels in the patients with transferred pulmonary adenocarcinoma or with non-transferred pulmonary adenocarcinoma and their changes with the treatment of radiotherapy. Results the patients with lung adenocarcinoma and non lung adenocarcinoma were significantly higher than that of COPD and health group,and patients with lung adenocarcinoma is significantly higher than patients with non lung adenocarcinoma (P<0.05);Integrin beta 1,VEGF and CD4+CD29+T cells,TNF-αand IL-1 level in patients with lung adeno-carcinoma metastasis were significantly higher than non-transferred group(P < 0.05);After radiotherapy,CD4+CD29+T cells,TNF-αand IL-1 in patients with lung adenocarcinoma were significantly lower than before(P<0.05);CD4+ CD29+ T cells,TNF alpha and IL-1 with integrin beta 1 and VEGF had significantly positive correlations. Conclusion CD4+CD29+T cells and cytokines increase significantly in the blood of patients with lung adenocarci-noma,and are related to the prognosis of metastasis and radiation therapy,which has important clinical significance.

3.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-427805

RESUMO

Objective To analyze the effect of iodine-131I in the treatment of patients with hyperthyroid heart disease(HHD).Methods The clinical materials and therapeutic effect by 131 I were reviewed in 100 patients with HDD.Results The heal rate of hyperthyroidism and HHD were 82.3%,86.5% in treatment group,and were higher than that of the control group (69.0% and 76.2% ) ( x2 =3.80,3.83,P < 0.05 ) ; HHD with atrial fibrillation was 65.0%,average cardioversion after 131I treatment was 74.4% after the treatment by 131I;The LVEDD、LVESD、LVEDV and HR after 131 I treatment were lower compared with before treatment ( all P < 0.05 ),SV and EF were increased ( all P < 0.01 ).Conclusion 131I treatment in patients with HHD,can significantly improve the efficacy of a heart disease

5.
J Exp Clin Cancer Res ; 27: 27, 2008 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-18694522

RESUMO

The c-Myc and human telomerase reverse transcriptase gene (hTERT) gene are frequently deregulated and overexpressed in malignancy. hTERT activity is induced by c-Myc and strategies designed to inhibit c-Myc expression in cancer cells may have considerable therapeutic value. We designed and used a short hairpin RNA to inhibit c-Myc expression in Colo 320 cells and validated its effect on cell proliferation. In this study, four c-Myc-shRNA expression vectors were constructed and introduced into Colo 320 cells. The effects of c-Myc silencing on tumor cell growth was assessed by soft agar assay and DNA synthesis experiments. The expressions of c-Myc and hTERT were also assessed by real-time reverse transcription-polymerase chain reaction and Western blot analysis. Upon transient transfection with plasmid encoding shRNA, it was found that expression of c-Myc and hTERT decreased in shRNA-transfected cells. The downregulation of c-Myc and hTERT inhibited cell growth, shortened telomere lengths, and suppressed telomerase activity. In conclusion, our findings demonstrate that shRNA of c-Myc can inhibit the DNA replication in Colo 320 cells effectively and reduce telomere length and telomerase activity, therefore, it could be used as a new potential anticancer tool for therapy of human colon cancer.


Assuntos
Neoplasias do Colo/genética , Regulação para Baixo , Proteínas Proto-Oncogênicas c-myc/antagonistas & inibidores , Interferência de RNA , Telomerase/genética , Linhagem Celular Tumoral , Proliferação de Células , Neoplasias do Colo/metabolismo , Neoplasias do Colo/patologia , Humanos , Proteínas Proto-Oncogênicas c-myc/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Telomerase/metabolismo , Telômero/metabolismo , Transfecção
6.
Cancer Biother Radiopharm ; 23(2): 229-37, 2008 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-18454692

RESUMO

Human colon cancer is the leading cause of cancer death in both men and women worldwide. The c-Myc gene is frequently deregulated and overexpressed in this malignancy, and strategies designed to inhibit c-Myc expression in cancer cells may have considerable therapeutic value. We design and use short hairpin RNA (shRNA) to inhibit c-Myc expression in Colo 320 cells and validat its effect on cell proliferation. In this study, four c-Myc-shRNA expression vectors were constructed and introduced into Colo 320 cells, and the cell cycle and apoptotic cells were analyzed by flow cytometry. The effects of c-Myc silencing on tumor-cell growth was assessed by the soft agar assay and by DNA synthesis experiments. Expression of c-Myc was also assessed by real-time reverse transcription polymerase chain reaction and Western blot analysis. Upon transient transfection with plasmid-encoding shRNA, it was found that expression of c-Myc decreased in shRNA-transfected cells, and the downregulation of c-Myc inhibited cell growth and induced apoptosis in Colo 320 cells. c-Myc downregulation also increased cell population in the G0-G1 phase. In conclusion, our findings demonstrate that shRNA can inhibit the DNA replication and induce apoptosis in Colo 320 cells effectively and, therefore, could be used as a new potential anticancer tool for the therapy of human colon cancer.


Assuntos
Neoplasias do Colo/metabolismo , Neoplasias do Colo/patologia , Proteínas Proto-Oncogênicas c-myc/deficiência , Proteínas Proto-Oncogênicas c-myc/genética , Interferência de RNA , Sequência de Bases , Linhagem Celular Tumoral , Proliferação de Células , Neoplasias do Colo/genética , Neoplasias do Colo/terapia , Regulação para Baixo , Regulação Neoplásica da Expressão Gênica , Vetores Genéticos/genética , Humanos , Dados de Sequência Molecular , Proteínas Proto-Oncogênicas c-myc/metabolismo
7.
Chem Biol Interact ; 170(3): 145-52, 2007 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-17764668

RESUMO

In order to evaluate mechanisms of natural plant purslane herb aquenous extracts (PHAS) for neuroprotective, we assessed neuroprotective effects of PHAS at doses of 2.5, 5 and 10 mg/(kg day) on SD mice injected daily with D-gal (50 mg/(kg day)) by behavioral tests. PHAS-fed mice showed higher activity upon induction by new environmental stimuli, lower anxiety and higher novelty-seeking behavior in the open field tasks, and significantly improved learning and memory ability in step-through compared with D-gal-treated mice. We further examined the mechanisms involved in neuroprotective effects of PHAS on mouse brain. PHAS significantly increased superoxide dismutase (SOD) activity and decreased the malondialdehyde (MDA) level. Meanwhile, PHAS also could up-regulate telomere lengths and telomerase activity in PHAS-fed groups. Furthermore, we examined the expression of p21(waf1) and p53 mRNA and protein in mouse brain by western blot analysis and real-time RT-PCR. We found that p21(waf1)was down-regulated by PHAS without changing the expression of p53. The results of this study suggested that the PHAS might be a primary target of p21(waf1)and the neuroprotective effect of PHAS might be carried out through a p21(waf1)-dependent and p53-independent pathway.


Assuntos
Galactose/toxicidade , Neurônios/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Portulaca/química , Animais , Comportamento Animal/efeitos dos fármacos , Inibidor de Quinase Dependente de Ciclina p21/metabolismo , Masculino , Malondialdeído/metabolismo , Camundongos , Fármacos Neuroprotetores/química , Fármacos Neuroprotetores/metabolismo , Extratos Vegetais/química , Superóxido Dismutase/metabolismo , Proteína Supressora de Tumor p53/metabolismo
8.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-536216

RESUMO

Objective To investigate the short and long term effect of mifepristone on hysteromyoma.Methods The treatment group ( n=60 ) was given mifepristone and the control group ( n=60 ) vitamin C.The volume of hysteromyoma was measured using B-mode ultrasound prior to and at the end of treatment.L H,FSH,E2 progesterone ( P) ,liver function and blood creatinine were monitored each month.At the second year,3 0 cases from treatmentgroup were given mifepristone again for 3 months in the same way as the first course and with the same indexes monitored. Results Mifepristone had1 0 0 % effective rate with one-course curative rate of6.67% ,the hysteromyoma volume decreased by an average of at least 3 5.1 0 % ,while the volume gradually increased over 6months after discontinuing mifepristone with the recurrence rate of3 0 .0 0 % .At the second course of treatment hysteromyoma was further reduced by50 .2 0 % ,with the scope of reduction larger than thatatthe firstcourse( P

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