Mena as a key enhancer factor of EMT to promote metastasis of human tongue squamous cell carcinoma
Hao CuiLiang XiangYifei ZhuSadam Ahmed ElayahHong QiLinyang XieZ G GuoFang SiyaMing YuYuxin GongJunbo TuSijia Na
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The aim of this study was to investigate the effect of mammalian-enabled (Mena) on tongue squamous cell carcinoma (TSCC) metastasis and its mechanism.Keywords:
Immunochemistry
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Intermediate Filament Protein
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Cell migration and mechanics are tightly regulated by the integrated activities of the various cytoskeletal networks. In cancer cells, cytoskeletal modulations have been implicated in the loss of tissue integrity, and acquisition of an invasive phenotype. In epithelial cancers, for example, increased expression of the cytoskeletal filament protein vimentin correlates with metastatic potential. Nonetheless, the exact mechanism whereby vimentin affects cell motility remains poorly understood. In this study, we measured the effects of vimentin expression on the mechano-elastic and migratory properties of the highly invasive breast carcinoma cell line MDA231. We demonstrate here that vimentin stiffens cells and enhances cell migration in dense cultures, but exerts little or no effect on the migration of sparsely plated cells. These results suggest that cell-cell interactions play a key role in regulating cell migration, and coordinating cell movement in dense cultures. Our findings pave the way towards understanding the relationship between cell migration and mechanics, in a biologically relevant context.
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It has been discovered that hepatocellular carcinoma (HCC) has high ability of migration and angiogenesis. This study aimed to explore the mechanism of HCC cell migration and angiogenesis. BEL-7402 cell line was used as HCC cell model for investigating the regulation of cell migration upon c-Src inhibitors (PP2 and SU6656) treatment. Western blot was used for detecting the expression of MT1-MMP and VEGF-C. The activity of MMP2 and MMP9 was monitored with gelatin zymography assay. BEL-7402 cell migration and invasion was detected by wound healing assay and Transwell. Immunoprecipitation was used for detecting the interaction among c-Src, pro-MT1-MMP, Furin and VEGF-C. Our results have show that the expression of MT1-MMP and VEGF-C were inhibited by PP2 and SU6656, in accordance with c-Src activity. Zymography assay demonstrated that the activity of MMP2 and MMP9 decreased upon PP2 or SU6656 treatment. The invasion and migration of BEL-7402 were inhibited. We also found that c-Src interacted with Furin in vivo. The interaction between Furin and its substrates pro-MT1-MMPã€pro-VEGF-C decreased upon c-Src inhibitors treatment. These findings indicate that the activity of c-Src inhibition associated with cell invasion and migration decreased by down-regulating the interaction between Furin and its substrates (pro-MT1-MMP, pro-VEGF-C). Key words: Hepatocellular carcinoma (HCC), Furin, c-Src inhibitor, MT1-MMP, VEGF-C, cell migration.
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The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation results in the synchronized response of cell migration on the villi. We conclude that cell proliferation within the crypt is the primary force that drives cell migration along the villus. This methodology can be applied to interrogate intestinal epithelial dynamics and characterize situations in which processes involved in cell turnover become uncoupled, including pharmacological treatments and disease models.—Parker, A., Maclaren, O. J., Fletcher, A. G., Muraro, D., Kreuzaler, P. A., Byrne, H. M., Maini, P. K., Watson, A. J. M., Pin, C. Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi. FASEB J. 31, 636–649 (2017). www.fasebj.org
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Vimentin is an important cytoskeleton protein for the biological function of macrophages. Alterations of vimentin filaments of CP-activated macrophages stained with FITC-labeled anti-vimentin antibody were observed under immunofluorescence microscope. Activated macrophages showed changes with the following characteristics: the intensity of immunofluorescence of vimentin was increased; the filaments of vimentin became thicker than those of normal macrophages when they were treated with colchicine; and the arrangement of vimentin filaments was parallel in direction to the polarization of the activated macrophages.
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Cell polarity
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Glioblastoma multiforme (GBM) has a high recurrence and mortality rate. Because of a poor understanding of the mechanism for this disease, treatment regimens have remained limited. Vimentin, one of the major cytoskeletal proteins, is associated with cellular structure. However, the function of vimentin in GBM is still undefined. In the present study, we investigated the expression level of vimentin in 179 GBM tissues using immunohistochemistry. We found that the vimentin expression level was associated with the time to progression ( P =0.029). A Kaplan-Meier analysis revealed that patients with high vimentin expression had a significantly shorter overall survival ( P =0.0002) and progression-free survival ( P =0.0001) compared with those with low expression. Furthermore, in vitro experiments showed that withaferin-A, a chemical inhibitor of vimentin, could inhibit GBM cell migration and invasion activity when its concentrations were <0.5 μM, and higher concentrations of withaferin-A could decrease the viability of U251and U87 cells significantly. In conclusion, our results indicated that vimentin may play an important role in the progression of GBM.
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Purpose. To study the expression of vimentin on the impact of dexamethasone (Dex) in human lens epithelial cells (HLECs), and the role of vimentin expression in steroid-induced cataract (GIC) formation. Material and methods. HLECs were exposed to DMEM and DMEM + 1umol/L Dex for 7 days. Real-time PCR and Western-blot were applied to identify the expression of vimentin at protein and transcription levels. The distribution and expression of vimentin in HLECs were measured by immumoflorescence staining. Results . Real-time PCR results showed that Dex group than the control group vimentin mRNA expression is decreased significantly different between groups (p<0.05), the difference was statistically significant. Western-blot results show that Dex group than the control group vimentin protein expression is decreased significantly different between groups (p<0.05), the difference was statistically significant, suggesting Dex can reduce the expression of vimentin. Immunofluorescence staining showed that Dex group than the control group vimentin expression is decreased significantly, which consistent with the Western-blot results. Conclusion. Dex can induce expression of vimentin in HLECs, which may cause abnormal lens epithelial cell proliferation and differentiation, eventually leading to the formation of GIC.
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