The effect of CDK4/6 inhibition on the expression of ribosomal protein RPL22L1 and FAU genes in the glioblastoma T98 cell line

Glioblastoma (GBM), an aggressive primary brain tumour, has a poor prognosis. There is still no complete cure for the disease. In GBM, ribosomal biogenesis is observed to be quite active and rapid compared to healthy cells. Cell cycle control proteins play a role in the regulation of ribosomal biogenesis. Overexpression of the ribosomal protein RPL22L1 is implicated in the emergence of aggressive phenotypes and is proposed as a new oncogene candidate. It has been suggested that RPL22L1 plays a role in cell proliferation, invasion, and migration and is associated with poor prognosis in GBM. The FAU protein, which is reported to be proapoptotic, is shown to be co-expressed with RPL22L1 in the STRING database. New strategies are being developed regarding the potential of ribosomal biogenesis control as a treatment in cancer. There is no information on the possible roles of RPL22L1 and FAU in GBM pathology. This study aimed to investigate the effects of Ribociclib, a new-generation CDK4/6 inhibitor, on RPL22L1 and FAU in U87 and T98G cell lines and its potent antitumour activity in resistant GBM. In this study, it was clearly determined that Ribociclib treatment applied to both U87 and T98G cell lines had an effect on cell viability in both cell lines. Wound healing analysis showed that T98G was more affected by Ribociclib compared to U87 cell lines. Our results obtained preliminary findings that Ribociclib may have a direct or indirect anticancer effect in GBM by causing changes in the possible gene expression of RPL22L1 and FAU proteins, which play an active role in ribosomal biogenesis, and/or by interacting with different cellular proteins. Further studies are required to support these findings.