Then, we investigated whether PTBP1 degradation was mediated by the proteasome using MG132, a specific proteasome inhibitor, and the results showed that the degradation of endogenous PTBP1 in GC cells with CCAT1 knockdown was prevented by MG132, suggesting that CCAT1 was involved in the post-translational regulation of PTBP1 (Fig. 6G). Here, PTBP1 is linked to gastric cancer.