Conclusions
USP38 might be a new therapeutic target for glioma.
Material and methods
USP38 overexpression and knockdown vector were constructed using the molecular clone method. The viability rate of U-87MG and U-138MG cells were detected using the Cell Counting Kit-8 (CCK-8) method.The expression and secretion of metastasis-related molecules were detected using the qPCR and ELISA method. The expression of metastasis-related molecules and JAK2/STAT3 signalling pathway was detected using western blotting analysis.
Methods
USP38 overexpression and knockdown vector were constructed using the molecular clone method. The viability rate of U-87MG and U-138MG cells were detected using the Cell Counting Kit-8 (CCK-8) method.The expression and secretion of metastasis-related molecules were detected using the qPCR and ELISA method. The expression of metastasis-related molecules and JAK2/STAT3 signalling pathway was detected using western blotting analysis.
Results
In this study, we firstly constructed a USP38 overexpression and inhibition model in 2 cell lines and found that overexpression of USP38 inhibits the viability rate and migration ability of glioma cells. We further noticed that elevated expression of USP38 reduced the expression and secretion of cell adhesion-related molecules with the elevation in expression of pro-apoptotic proteins, and these effects might be mediated by inhibition of JAK2/STAT3 signalling pathway as USP38 is the upstream regulator of STAT3 and inhibition of cellular adhesion process. Conclusions: USP38 might be a new therapeutic target for glioma.