Conclusion
Therefore, RPSAP52 upregulates TGF-β1 to increase cancer cell stemness and predict postoperative survival in GBM.
Methods
A total of 50 GBM patients (33 males and 20 females; 54-75 years; mean age: 61.8±5.8 years) were selected from the 89 cases of GBM patients. Under the guidance of MRI, brain biopsy was performed to collect GBM tissues from each patient for the diagnosis of GBM. U-373 MG cells were employed and had transient transfections. qRNA, Western blot, and a series of experiments were performed to characterize their associations.
Results
The results showed that RPSAP52 was upregulated in GBM patients, and its high expression levels predicted poor survival. In GBM tissues, expression levels of RPSAP52 were significantly and positively correlated with that of TGF-β1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β1 attenuated the effects of RPSAP52 siRNA silencing.