Background: The purpose of this study is to explore the role and mechanism of MMP-9 in the EMT process of thyroid cancer (TC), so as to provide a basis for clinical exploration of invasion and metastasis process of TC, looking for biological markers of tumor metastasis and molecular intervention therapy. Methods: Western blot and RT-PCR were employed to detect the expression of MMP-9 in human normal thyroid cell line HT-ori3 and human TC cell lines IHH-4 (PTC), FTC-133, and 8505C. Expression levels of EMT-related markers: epithelial cell marker E-cadherin and stromal cell marker Vimentin in TGF-1-induced TC cell lines were detected by Western blot and RT-PCR, respectively. The effects of MMP-9 downregulation on cell invasion and metastasis were investigated by wound-healing assay and cell invasion experiment. Results: The protein and mRNA expression levels of MMP-9 in TC cell lines were increased compared with the human normal thyroid cell line HT-ori3. When TGF-β1 was added, the expression of EMT and Vimentin increased while the expression of E-cadherin decreased. Compared with the control group, the TC cells stably transfected with MMP-9 shRNA showed inhibited EMT, decreased Vimentin expression, and increased E-cadherin expression. The induction of TGF-β1 did not promote the occurrence of EMT in TC cells which were stably transformed with MMP-9 shRNA. The addition of TGF-β1 to TC cells increased the ability of the cells to migrate and invade. Compared with the control group, the migration and invasion ability of TC cells stably transfected with MMP-9 shRNA was significantly reduced, and the induction of TGF-β1 could not restore the migration and invasion ability of cells without MMP-9. Conclusions: In conclusion, we found that MMP-9 can be used as a biomarker for TC, which can promote the EMT process of TGF-β1 induced TC, and thus affecting the cell migration and invasion ability.
Background The purpose of this study is to explore the role and mechanism of MMP-9 in the EMT process of thyroid cancer (TC), so as to provide a basis for clinical exploration of invasion and metastasis process of TC, looking for biological markers of tumor metastasis and molecular intervention therapy.Methods Western Blot and RT-PCR were employed to detect the expression of MMP-9 in human normal thyroid cell line HT-ori3 and human TC cell lines IHH-4 (PTC), FTC-133 and 8505C. Expression levels of EMT-related markers: epithelial cell marker E-cadherin and stromal cell marker Vimentin in TGF-1-induced TC cell lines were detected by Western Blot and RT-PCR, respectively. The effects of MMP-9 down-regulation on cell invasion and metastasis were investigated by wound-healing assay and cell invasion experiment.Results The protein and mRNA expression levels of MMP-9 in TC cell lines were increased compared with human normal thyroid cell line HT-ori3. When TGF-β1 was added, the expression of EMT and Vimentin increased while the expression of E-cadherin decreased. Compared with the control group, the TC cells stably transfected with MMP-9 shRNA showed inhibited EMT, decreased Vimentin expression and increased E-cadherin expression. The induction of TGF-β1 did not promote the occurrence of EMT in TC cells which were stably transformed with MMP-9 shRNA. The addition of TGF-β1 to TC cells increased the ability of the cells to migrate and invade. Compared with the control group, the migration and invasion ability of TC cells stably transfected with MMP-9 shRNA was significantly reduced, and the induction of TGF-β1 could not restore the migration and invasion ability of cells without MMP-9.Conclusions In conclusion, we found that MMP-9 can be used as a biomarker for TC, which can promote the EMT process of TGF-β1 induced TC, and thus affecting the cell migration and invasion ability.
To discuss the mechanism of miR-134 in improving cognitive function of VD rats through regulating the oxidative stress and autophagy and reducing the expression of Cofilin 2. VD rats was established. They were disposed with miR-134 antagonist. The cerebral regulatory capacity was observed through ethology. The pathological change in CAI area of hippocampus and cerebral cortex was observed with HE staining method. The regulation of miR-134 targeting downstream was analyzed through bioinformatics. The presentation level of SOD, GSH, ROS and MDA was detected. The expression of LC1/LC-3 and p62 was detected with Western Blot assay. There was visible activated microglial cells and gliocyte proliferation in VD rat’s model. The myelination was weakened. They were improved notably through the treatment with miR-134 antagonist. The expression of MDA and ROS could be restrained by miR-134 antagonist through reducing the expression of Cofilin 2. The expression of SOD and GSH could be increased and oxidative stress could be reduced. The level of autophagy could be decreased. The cognitive function of VD rats could be improved by miR-134 antagonist through regulating the oxidative stress and autophagy and reducing presentation of Cofilin 2.
We investigated the effect of GSK-3β RNAi lentivirus on neuronal damage and Nrf2 level in rats with cerebral infarction. 40 rats were assigned into sham group, CI group, Vector group and GSK-3β RNAi group followed by analysis of cell damage and oxidative stress, neurological scores, cerebral infarction volume, and brain water content as well as brain morphology by H&E staining and Nrf2 protein level by Western blot. Compared with sham group, GSK-3β mRNA in neurons of CI group and Vector group was significantly elevated (P < 0.05) with reduced level in GSK-3β RNAi group (P < 0.05); 3 hours after surgery, there was no change in neuroethology scores of rats in CI group, Vector group and GSK-3β RNAi group (P > 0.05). While 1 and 3 days later, the scores of rats were significantly improved (P < 0.05) and brain water content was reduced in GSK-3β RNAi group (P < 0.05) without difference between CI group and Vector group (P > 0.05). Compared with sham group, infarct size in CI group and Vector group was increased (P < 0.05) and reduced in GSK-3β RNAi group (P < 0.05) without difference between CI group and Vector group (P > 0.05). Meanwhile, CI group and Vector group showed significantly downregulated Nrf2, Srx1 and Trx1 proteins (P < 0.05), which were increased in GSK-3β RNAi group (P < 0.05). In conclusion, GSK-3β RNAi lentivirus can promote the expression of Nrf2 and exert an inhibitory effect on neurons of rats with cerebral infarction, therefore protecting brain tissue.
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