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Objective To discuss the effect and mechanism of miR-34a on the proliferation, apoptosis and invasion of laryngeal carcinoma cells. Methods The laryngeal squamous carcinoma Hep2 cells were transiently transfected with miR-34a mimics and miR-34a NC. The MTT, colony-forming assay, Hoechst staining and AnnexinV-PI double staining flow cytometry were employed to detect the effect of miR-34a on the viability and apoptosis of laryngeal squamous carcinoma Hep2 cells; Transwell assay to defect the effect of miR-34a on the migration and invasion of laryngeal squamous carcinoma Hep2 cells; western blot and RT-PCR assay to defect the effect of miR-34a mimics on the expression of survivin and Ki-67 mRNA in laryngeal squamous carcinoma Hep2 cells. Results Compared with miR-34a NC group, the cell viability in miR-34 mimics group was significantly decreased (P < 0.01), the cell apoptosis rate was significantly increased (P < 0.01), the abilities of cell migration and invasion were significantly reduced (P < 0.01) and the expression of survivin and Ki-67 mRNA was significantly decreased (P < 0.01). Conclusions The increased expression of miR-34a can induce the apoptosis of Hep2 laryngeal carcinoma cells and inhibit the cell proliferation and invasion, which is related to the down-regulated expression of survivin and Ki-67.
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OBJECTIVE@#To discuss the effect and mechanism of miR-34a on the proliferation, apoptosis and invasion of laryngeal carcinoma cells.@*METHODS@#The laryngeal squamous carcinoma Hep2 cells were transiently transfected with miR-34a mimics and miR-34a NC. The MTT, colony-forming assay, Hoechst staining and AnnexinV-PI double staining flow cytometry were employed to detect the effect of miR-34a on the viability and apoptosis of laryngeal squamous carcinoma Hep2 cells; Transwell assay to defect the effect of miR-34a on the migration and invasion of laryngeal squamous carcinoma Hep2 cells; western blot and RT-PCR assay to defect the effect of miR-34a mimics on the expression of survivin and Ki-67 mRNA in laryngeal squamous carcinoma Hep2 cells.@*RESULTS@#Compared with miR-34a NC group, the cell viability in miR-34 mimics group was significantly decreased (P < 0.01), the cell apoptosis rate was significantly increased (P < 0.01), the abilities of cell migration and invasion were significantly reduced (P < 0.01) and the expression of survivin and Ki-67 mRNA was significantly decreased (P < 0.01).@*CONCLUSIONS@#The increased expression of miR-34a can induce the apoptosis of Hep2 laryngeal carcinoma cells and inhibit the cell proliferation and invasion, which is related to the down-regulated expression of survivin and Ki-67.
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Objective: To investigate the mechanism of survivin, p53 and Ki-67 on Hep-2 human laryngeal cancer endothelial cell proliferation and invasion. Methods: Laryngeal squamous cell carcinoma and paracancerous normal tissues were collected, total RNA was extracted from tissues, survivin, p53 and Ki-67 gene mRNA expression levels in laryngeal cancer and the adjacent tissues were detected by Real-time PCR. Human laryngeal cancer Hep-2 epithelial cells were selected, survivin gene was overexpressed, and cell proliferation was detected by MTT. p53 and Ki-67 gene expression changes in overexpressed survivin gene were detected by Western blot. Changes in Hep-2 cell invasive ability were studied when survivin was overexpressed as detected by Transwell invasion assay. Results: In the adjacent tissues, survivin, p53 and Ki-67 gene relative expression levels were 1.72 ± 0.9, 13.7 ± 5.7 and 5.7 ± 1.3, respectively; while in cancer tissues, gene relative expression levels were 53.7 ± 8.3, 66.7 ± 5.2 and 61.0 ± 3.1, respectively, which was significantly increased. As detected by MTT, relative cell survival rate within 12 h of survivin overexpression were: load control group (88.5 ± 1.6)%; overexpressed group (90.3 ± 1.9)%. Transwell invasion assay results indicated that overexpressed survivin could significantly increase the relative survival rate of cells. Conclusions: Expressions of p53, Ki67 and survivin are increased in cancer; and there is a positive correlation between survivin, p53 and Ki67 expressions in laryngeal carcinoma.
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OBJECTIVE@#To investigate the mechanism of survivin, p53 and Ki-67 on Hep-2 human laryngeal cancer endothelial cell proliferation and invasion.@*METHODS@#Laryngeal squamous cell carcinoma and paracancerous normal tissues were collected, total RNA was extracted from tissues, survivin, p53 and Ki-67 gene mRNA expression levels in laryngeal cancer and the adjacent tissues were detected by Real-time PCR. Human laryngeal cancer Hep-2 epithelial cells were selected, survivin gene was overexpressed, and cell proliferation was detected by MTT. p53 and Ki-67 gene expression changes in overexpressed survivin gene were detected by Western blot. Changes in Hep-2 cell invasive ability were studied when survivin was overexpressed as detected by Transwell invasion assay.@*RESULTS@#In the adjacent tissues, survivin, p53 and Ki-67 gene relative expression levels were 1.72 ± 0.9, 13.7 ± 5.7 and 5.7 ± 1.3, respectively; while in cancer tissues, gene relative expression levels were 53.7 ± 8.3, 66.7 ± 5.2 and 61.0 ± 3.1, respectively, which was significantly increased. As detected by MTT, relative cell survival rate within 12 h of survivin overexpression were: load control group (88.5 ± 1.6)%; overexpressed group (90.3 ± 1.9)%. Transwell invasion assay results indicated that overexpressed survivin could significantly increase the relative survival rate of cells.@*CONCLUSIONS@#Expressions of p53, Ki67 and survivin are increased in cancer; and there is a positive correlation between survivin, p53 and Ki67 expressions in laryngeal carcinoma.
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<p><b>OBJECTIVE</b>Clinical studies have shown decreased levels of sexual hormones, particularly testosterone deficiency, in men with chronic heart failure (CHF). The authors aimed to investigate the effect of testosterone on cardiac function and the possible mechanism of androgen protecting the heart in male rats.</p><p><b>METHODS</b>Forty-three male SD rats were randomly divided into 3 groups: right heart failure (RHF, n = 15), physiologic testosterone treatment (TT, n = 15) and control (n = 13). The RHF group was given intraperitoneal injection of monocrotaline at 60 mg/kg to make RHF models; the TT group was injected with testosterone at 5 mg/kg 3 days after monocrotaline administration; and the control group received equal volume of saline. The CD34+ cells in the peripheral blood of each rat were counted by flow cytometry. The levels of serum testosterone and tumor necrosis factor alpha (TNF-alpha) were measured by chemiluminescence immunoassay and enzyme linked immunosorbent assay, respectively. The hearts, lungs and livers of all the surviving rats were excised at 6 weeks for pathological and immunohistochemical examinations.</p><p><b>RESULTS</b>The level of serum testosterone was gradually decreased, while that of TNF-alpha obviously increased in the RHF group. After testosterone treatment, the TT group showed a remarkable improvement of cardiac performance and a significant decrease in the level of serum TNF-alpha as compared with the RHF group. Statistically significant differences were observed neither in the CD34+ cell count in the peripheral blood nor in the CD34+ expression of the myocardial cells between the TT and RHF groups.</p><p><b>CONCLUSION</b>Physiological supplementation of testosterone can improve the cardiac function of RHF male rats, probably through its inhibition of TNF-alpha rather than by autologous mobilization of bone marrow stem cells.</p>
Subject(s)
Animals , Male , Rats , Heart Failure , Drug Therapy , Metabolism , Rats, Sprague-Dawley , Testosterone , Blood , Therapeutic Uses , Tumor Necrosis Factor-alpha , BloodABSTRACT
The aim of this study was to investigate the effect of the total saponins of Panaxginseng (TSPG) on cells expression of apoptosis-related genes bax and bcl-xl in HL-60 cells and its mechanism inducing apoptosis of HL-60 cells. The morphology of HL-60 cells was observed under normal and fluorescence microscopes; the percentage of apoptotic HL-60 cells was assayed by flow cytometry and the DNA ladder was observed by DNA agarose gel electrophoresis; the expression changes of bax and bcl-xl mRNAs were detected by RT-PCR after HL-60 cells were treated with TSPG at final concentrations of 0, 100, 200, 400, 800 and 1600 microg/ml for 48 hours. The results showed that the percentage of apoptotic HL-60 cells went up as the dose increased, the typical apoptotic cell morphology and the appearance of apoptotic DNA ladder could be observed when treated with 0 - 400 microg/ml TSPG for 48 hours. At the same time and same range of concentration, the expression of bax mRNA increased and the bcl-xl expression decreased gradually. When higher than 400 microg/ml of TSPG was used, cell necrosis appeared and the percentage of apoptotic HL-60 cells even decreased. It is concluded that the apoptosis or necrosis in HL-60 cells can be induced by TSPG at certain range of concentration, and the percentage of apoptosis is dose-dependent. The effect on up-regulation of bax mRNA and down-regulation of bcl-xl mRNA probably play an important role in apoptosis of HL-60 cells induced by TSPG.
Subject(s)
Humans , Apoptosis , HL-60 Cells , Panax , Chemistry , RNA, Messenger , Genetics , Metabolism , Saponins , Pharmacology , bcl-2-Associated X Protein , Genetics , MetabolismABSTRACT
Objective To increase the awareness of virus-associated hemophagocytic syndrome.Methods Sixteen cases of virus-associated hemophagocytic syndrome were retrospectively analyzed.Results All presented with persistent high fever,cytopenia,hepato-splenomegaly,hepatic dysfunction,hypertriglyceridemia,hyperferritinemia,coagulopathy,hypofibrinogenemia,cytokine storm and a low natural killer cell activity.All patients had lymphohistiocytic accumulation in bone marrow.Treatment with high-dose gamma-globulin and high-dose methylprednisolone.Clinical symptoms and laboratory improved,and five patients died.Conclusion Aggressive early diagnosis and treatment are critical to improve survival.