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Objective·To explore the effects of ubiquitin protein ligase E3C (UBE3C) on proliferation and invasion in epithelial ovarian cancer SKOV3 cells. Methods?·?Western blotting was used to detect the expression difference of UBE3C in epithelial ovarian cancer cell lines and normal ovarian cell lines. SKOV3 cells were transfected with si-UBE3C to knockdown UBE3C protein level, while ex-UBE3C plasmid was used to upregulate the expression of UBE3C. Cell proliferation was measured by CCK-8 assay and colony formation assay. Wound healing assay and Transwell assay were performed to investigate the effect of UBE3C on migration and invasion. Protein levels of β-catenin and c-Myc were also detected in different groups, which were closely related to proliferation and invasion. Results?·?UBE3C was highly expressed in epithelial ovarian cancer cell lines. UBE3C was successfully silenced with si-UBE3C transfection in SKOV3 cells. Inhibition of UBE3C significantly weakened the abilities of cell proliferation, migration and invasion. A reduction of β-catenin and c-Myc protein levels was also accompanied by UBE3C knockdown. Overexpression of UBE3C with ex-UBE3C plasmid promoted the abilities of proliferation, migration and invasion. Enhanced expression levels of β-catenin and c-Myc were also verified. Conclusion?·?UBE3C promotes proliferation and invasion of epithelial ovarian cancer SKOV3 cells. This might be to do with upregulation of β-catenin and c-Myc protein levels.
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Objective • To explore the effects of ubiquitin protein ligase E3C (UBE3C) on proliferation and invasion in epithelial ovarian cancer SKOV3 cells. Methods • Western blotting was used to detect the expression difference of UBE3C in epithelial ovarian cancer cell lines and normal ovarian cell lines. SKOV3 cells were transfected with si-UBE3C to knockdown UBE3C protein level, while ex-UBE3C plasmid was used to upregulate the expression of UBE3C. Cell proliferation was measured by CCK-8 assay and colony formation assay. Wound healing assay and Transwell assay were performed to investigate the effect of UBE3C on migration and invasion. Protein levels of β-catenin and c-Myc were also detected in different groups, which were closely related to proliferation and invasion. Results • UBE3C was highly expressed in epithelial ovarian cancer cell lines. UBE3C was successfully silenced with si-UBE3C transfection in SKOV3 cells. Inhibition of UBE3C significantly weakened the abilities of cell proliferation, migration and invasion. A reduction of β-catenin and c-Myc protein levels was also accompanied by UBE3C knockdown. Overexpression of UBE3C with ex- UBE3C plasmid promoted the abilities of proliferation, migration and invasion. Enhanced expression levels of β-catenin and c-Myc were also verified. Conclusion • UBE3C promotes proliferation and invasion of epithelial ovarian cancer SKOV3 cells. This might be to do with upregulation of β-catenin and c-Myc protein levels.
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<p><b>OBJECTIVE</b>To investigate the changes in the transcription of protein arginine methylation enzyme family genes in the dorsal root ganglia (DRG) following peripheral nerve injury in mice.</p><p><b>METHODS</b>C57BL6 mouse models of neuropathic pain induced by peripheral nerve injury were established by bilateral L4 spinal nerve ligation (SNL). At 7 days after SNL or sham operation, the DRG tissue was collected for transcriptional analysis of 9 protein arginine methylation enzyme genes (Prmt1?3, Carm1, and Prmt5?9) using RNA?Seq to identify the differentially expressed genes in the injured DRGs. We also established mouse models of lateral L4 SNL and models of chronic constriction injury (CCI) of the sciatic nerve and tested the paw withdrawal frequency (PWF) in response to mechanical stimulation and paw withdrawal latency (PWL) in response to thermal stimulation on 0, 3, 7 and 14 days after SNL or CCI; the expressions of the differentially expressed genes in the injured DRGs were verified in the two models using RT?qPCR.</p><p><b>RESULTS</b>Among the 9 protein arginine methylation enzyme family genes that were tissue?specifically expressed in the DRG, Prmt2 and Prmt3 showed the highest and Prmt6 showed the lowest basal expression. Compared with the sham?operated mice group, the mice receiving SNL exhibited upregulated Carm1 gene transcription (by 1.7 folds) but downregulated Prmt5, Prmt8 and Prmt9 transcription in the injured DRG (Prmt8 gene showed the most significant down?regulation by 16.3 folds). In mouse models of SNL and CCI, Carm1 gene expression increased progressively with time while Prmt8 transcription was obviously lowered on days 3, 7 and 14 after the injury; the transcription levels of Prmt1, Prmt5 and Prmt9 presented with no significant changes following the injuries. Both SNL and CCI induced mechanical allodynia and thermal hypersensitivities in the mice shown by increased PWF and decreased PWL on days 3, 7 and 14 after the injuries.</p><p><b>CONCLUSION</b>Periphery nerve injury induces Carm1 upregulation and Prmt8 downregulation in the injured DRG in mice, which sheds light on new targets for treatment of neuropathic pain.</p>
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<p><b>OBJECTIVE</b>To observe the protective effect of compound acanthopanax senticosus injection (CASI) on myocardial ischemia-reperfusion arrhythmia in rats.</p><p><b>METHOD</b>The myocardial ischemia-reperfusion model was induced by 30 min coronary occulusion and 60 min reperfusion in openchest anesthetized rats. The changes of arrhythmia with electrocardiogram lead II, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the contents of malondialdehyde (MDA) and Ca2+ in myocardium were determined.</p><p><b>RESULT</b>In rats treated by CASI (in a dosage of 25, 50 and 100 mg x kg(-1) femoral vein infusion at 30 min after coronary occulusion), the incidence of myocardial ischemia-reperfusion ventricular arrhythmias, for instance the ventricular tachycardia (VT) and ventricular fibrillation (Vf), was effectively prevented, the appearing time of arrhythmia was delayed and the duration of arrhythmia was shortened, while the elevated ST segment lowered as well. At the same time, the contents of myocardial Ca2+ and MDA were decreased significantly as well as the activities of myocardial SOD and GSH-Px increased markedly.</p><p><b>CONCLUSION</b>CASI is of protective effect on myocardial ischemia-reperfusion arrhythmia, which may be related to scavenging the oxygen free radicals and Ca2+ overload formed during reperfusion.</p>