In conclusion, the downregulation of HspB1, BTF3, PGAM1 and cofilin bring new insights in CM16 antiproliferative effects, further supporting CM16 as an interesting protein synthesis inhibitor to combat glioma.
These data indicate that the expression of PGAM1 is increased in C6 cells and human astrocytomas, and PGAM1 is probably involved in the tumorigenesis and progression of glioma, which may be a potential target for glioma treatment.
Interestingly, triose phosphate isomerase (TPI), phosphoglycerate mutase 1 (PGAM1), adaptor molecule (CRK2), protein DJ-1 (PARK7) and basic transcription factor 3 (BTF3) were found to be down-regulated and can be studied further to understand their therapeutic potential in gliomas.