| Background and objective:There are many challenges in the current treatment of gliomas.High-grade gliomas show intratumoral and intertumoral heterogeneity that makes chemoradiotherapy resistant and relapse with tumors.Relative to these problems,drug combination therapy has shown more and more advantages.Large-scale genomic and proteomic analysis of gliomas can identify potential drug targets.Targets for "available drugs" can be identified as clinical drug candidates after validation.Studying the molecular mechanism of gliomas and exploring the corresponding targeted drugs are urgent problems that need to be addressed in the treatment of gliomas today.EMT is closely related to tumorigenesis,malignant progression,and resistance of tumor cells to treatment.Recent studies have shown that EMT occurs in a gradual manner,which is characterized by cells expressing different levels of epithelial and mesenchymal cell markers and their epigenetic differences.The process of EMT is reversible.Tumor cells that have undergone the EMT process can invade adjacent tissues.Once they enter the blood or lymphatic vessels,they can cooperate with non-EMT cells to complete tumor metastasis and colonization in distant organs.NC is a component extracted from the roots of the two-needle needles of the Zanthoxylum plant distributed in northeastern Asia,and has a variety of biological activities.Recent studies have shown that NC can inhibit tumor cell proliferation and EMT in various tumors.However,the inhibitory effect of NC on glioma cell EMT and its mechanism have not yet been elucidated,and no one has explored it.The purpose of this study was to investigate the inhibitory effect of NC on human glioma cell EMT and its possible molecular mechanism.Methods:TGF-β1 was used to induce EMT changes in glioma cells,and NC was used as an intervention drug for glioma EMT.Through Western blotting,Transwell invasion assay,flow cytometry experiments and other methods,the mechanism of the inhibitory effect of NC on EMT in gliomas was analyzed and studied.Results:1.The survival rate of glioma cells decreased with the addition of NC,suggesting that NC inhibited the proliferation of glioma cells.2.NC suppressed the expression of EMT-related protein markers in glioma cells,indicating that can inhibit the occurrence of EMT in gliomas.3.NC inhibit the ability of glioma cells to migrate and invade,indicating that can inhibit the migrate and invade of EMT in gliomas.4.NC increased the apoptosis rate of glioma cells and enhanced the expression of related apoptotic proteins,indicating that NC inhibited the growth of glioma cells by promoting the apoptosis of glioma cells.5.The expression of EMT-related protein markers decreased after the addition of specific STAT3 inhibitors,suggesting that NC repressed the occurrence of glioma EMT by inhibiting the transcription factor STAT3.Conclusions:1.NC has a concentration-dependent inhibitory effect on the proliferation of glioma LN18 and U87 cells.2.NC inhibits EMT glioma in LN18 and U87 cells.3.NC can significantly repress the cell migration and invasion ability of EMT in glioma cells.4.NC is able to promote the glioma cell apoptosis.5.STAT3 involved in EMT of glioma cells,and the supression effect of NC on EMT in glioma cells by reducing activity of STAT3. |
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