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1.
Academic Journal of Second Military Medical University ; (12): 878-882, 2015.
Article in Chinese | WPRIM | ID: wpr-838993

ABSTRACT

Objective To evaluate the effect of apigenin on cell migration, invasion of human lung cancer cell line A549 and the underlying mechanisms. Methods A549 cells were cultured with different concentrations of apigenin (0, 5, 10, 20, 40, 80, and 160 μmol/L), and CCK8 assay was used to evaluate the cell inhibition rates. Cell migration and invasion capabilities were evaluated by means of transwell and transwell matrix penetration assays. Enzyme-linked immunosorbent assay (ELISA) and Western blotting analysis were used to study the activities and expressions of invasion-related proteins matrix-metallopeptidase 2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF). Results CCK8 assay results showed that apigenin caused a concentration-dependent (40, 80, and 160 μmol/L) inhibition against proliferation of A549 cells (P <0.05). Compared with the control group, apigenin significantly inhibited the migration and invasion capabilities of A549 cells, accompanied by significantly decreased MMP-2 and VEGF expression (P <0.05). However, apigenin showed no effect on MMP-9 protein expression. Conclusion Apigenin can effectively inhibit migration and invasion of human lung cancer cell line A549, which is probably through suppressing the expressions of MMP-2 and VEGF.

2.
Tumor ; (12): 24-30, 2015.
Article in Chinese | WPRIM | ID: wpr-848740

ABSTRACT

Objective: To investigate the effects of phosphoinositide-3 kinase, catalytic subunit delta (PIK 3CD ) gene silencing on the proliferation and migration of human gastric cancer HGC-27 cells in vitro and its possible mechanism. Methods: The expression level of PIK3CD mRNA in HGC-27 cells was detected by real-time fluorescent quantitative PCR. HGC-27 cells were transfected with recombinant plasmid MSCV-PIK3CD-shRNA, then the expression silencing of PIK 3CD gene was verified by real-time fluorescent quantitative PCR and Western blotting. The proliferation and migration abilities of HGC-27 cells after transfection with MSCV-PIK3CD-shRNA were detected by cell count kit-8 (CCK-8) assay and Transwell chamber assay, respectively. The expressions of Akt signal pathwayrelated proteins in HGC-27 cells after transfection with MSCV-PIK3CD-shRNA were detected by Western blotting. Results: The expression level of PIK3CD mRNA in gastric cancer HGC-27 cells was higher than that in normal gastric mucosal GES-1 cells. After transfection with MSCV-PIK3CD-shRNA, the expression levels of PIK3CD mRNA and protein in HGC-27 cells with high expression of PIK 3CD gene were significantly decreased (P < 0.05), and the cell proliferation and invasive abilities were significantly reduced (P < 0.05). PIK 3CD gene silencing had no effect on the expression of Akt, but significantly inhibited the expression of phospho-Akt (p-Akt) (P < 0.05). Conclusion: PIK3CD may promote the proliferation and migration of gastric cancer HGC-27 cells in vitro by activating Akt pathway.

3.
Tianjin Medical Journal ; (12): 133-136, 2015.
Article in Chinese | WPRIM | ID: wpr-461207

ABSTRACT

Objective To investigate the inhibiting effects of alcohol extract from Dioscore bulbifera on proliferation, colony formation and migration of cancer cell lines. Methods Alcohol extract from Dioscore bulbifera was prepared using Soxhlet extraction. Human gastric cancer cell line MGC803 was treated with different concentrations(0, 60, 120 mg/L)of al?cohol extract from Dioscore bulbifera. In vitro, proliferation, colony formation and migration of gastric cancer cells were detect?ed by MTT, colony formation experiments and Transwell assay respectively. Results The proliferation(day2-day 6, F=29.130, 21.864, 67.826, 36.015, 43.656, P<0.01)and colony formation(F=11.918,P<0.01)of gastric cancer cells were significantly inhibited by administration of alcohol extract from Dioscore bulbifera at both 60 mg/L and 120 mg/L . The migra?tion(F=4.258,P<0.05)of gastric cancer cells were significantly suppressed after cells were treated with120 mg/L alcohol ex?tract from Dioscore bulbifera. Conclusion Alcohol extract from Dioscore bulbifera significantly inhibit proliferation, colony formation and migration of gastric cancer cells.

4.
Clinics ; 69(2): 134-144, 2/2014. graf
Article in English | LILACS | ID: lil-701378

ABSTRACT

OBJECTIVE: The present study aimed to investigate the mechanisms underlying the anti-inflammatory and anti-angiogenic effects of ethyl-p-methoxycinnamate isolated from Kaempferia galanga. METHODS: The anti-inflammatory effects of ethyl-p-methoxycinnamate were assessed using the cotton pellet granuloma assay in rats, whereby the levels of interleukin-1 and tumor necrosis factor-α were measured in the animals' blood. In addition, the levels of interleukin, tumor necrosis factor, and nitric oxide were measured in vitro using the human macrophage cell line (U937). The analgesic effects of ethyl-p-methoxycinnamate were assessed by the tail flick assay in rats. The anti-angiogenic effects were evaluated first by the rat aortic ring assay and, subsequently, by assessing the inhibitory effects of ethyl-p-methoxycinnamate on vascular endothelial growth factor, proliferation, migration, and tube formation in human umbilical vein endothelial cells. RESULTS: Ethyl-p-methoxycinnamate strongly inhibited granuloma tissue formation in rats. It prolonged the tail flick time in rats by more than two-fold compared with the control animals. The inhibition of interleukin and tumor necrosis factor by ethyl-p-methoxycinnamate was significant in both in vivo and in vitro models; however, only a moderate inhibition of nitric oxide was observed in macrophages. Furthermore, ethyl-p-methoxycinnamate considerably inhibited microvessel sprouting from the rat aorta. These mechanistic studies showed that ethyl-p-methoxycinnamate strongly inhibited the differentiation and migration of endothelial cells, which was further confirmed by the reduced level of vascular endothelial growth factor. CONCLUSION: Ethyl-p-methoxycinnamate exhibits significant anti-inflammatory potential by inhibiting pro-inflammatory cytokines and angiogenesis, thus inhibiting the main functions of endothelial cells. Thus, ethyl-p-methoxycinnamate could be a promising therapeutic agent ...


Subject(s)
Animals , Humans , Male , Rats , Angiogenesis Inhibitors/pharmacology , Anti-Inflammatory Agents/pharmacology , Cinnamates/pharmacology , Plant Extracts/pharmacology , Vascular Endothelial Growth Factor A/drug effects , Zingiberaceae/chemistry , Analysis of Variance , Angiogenesis Inhibitors/isolation & purification , Anti-Inflammatory Agents/isolation & purification , Cell Proliferation/drug effects , Enzyme-Linked Immunosorbent Assay , Human Umbilical Vein Endothelial Cells/drug effects , Interleukin-1/analysis , Rats, Sprague-Dawley , Reproducibility of Results , Tumor Necrosis Factor-alpha/analysis , Tumor Necrosis Factor-alpha/drug effects , /drug effects , Vascular Endothelial Growth Factor A/analysis
5.
Tumor ; (12): 398-403, 2013.
Article in Chinese | WPRIM | ID: wpr-848996

ABSTRACT

Objective: To investigate the effects of miR(microRNA)-200a on migration and invasion abilities of glioma cells, and to explore its possible mechanism. Methods: Differential expression levels of miR-200a in glioma U87 cells were achieved by transfecting with hsa-miR-200a mimic, hsa-miR-200a inhibitor or hsa-miR-negative control by Lipofectamine™ 2000. The migration and invasion abilities of U87 cells were detected by wound-healing assay and Transwell invasion assay, respectively. Bioinformatics software was used to predict downstream target genes of miR-200a and their binding sites. The potential target genes were verified by Luciferase Reporter Assay and Western blotting. Results: Exogenous overexpression of miR-200a could promote migration and invasion abilities of U87 cells (P < 0.05), while miR-200a inhibitors could generate the opposite results (P < 0.05). Luciferase Reporter Assay and Western blotting revealed that hsa-miR-200a negatively regulated the protein expression of NCAM1 (neural cell adhesion molecule 1) gene which was regarded as the target gene. Conclusion: The miR-200a can promote the migration and invasion abilities of glioma U87 cells, in which NCAM1 may be one of the target genes. Copyright © 2013 by TUMOR.

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