Methionine deprivation inhibits glioma proliferation and EMT via the TP53TG1/miR-96-5p/STK17B ceRNA pathway

Abstract

Abstract Recent research highlights the significant impact of methionine metabolism on glioma progression. An increasing amount of compelling evidence bridges long non-coding RNAs to abnormal metabolism in gliomas. However, the specific role of long non-coding RNAs in methionine metabolism regulating glioma progression remains unclear. This study reveals that methionine deprivation inhibits the proliferation, migration, and invasion capabilities of gliomas. Interestingly, the expression of TP53TG1, a long non-coding RNA, is also suppressed. TP53TG1 is highly expressed in gliomas and associated with poor patient outcomes. Subsequently, our data proves that inhibition of TP53TG1 suppresses glioma cell proliferation and the epithelial-mesenchymal transition process both in vitro and in vivo. Ultimately, we found that the underlying mechanism involves a competing endogenous RNA regulating network, in which TP53TG1 modulates the target protein STK17B by competitively binding to miR-96-5p, thus regulating glioma progression. These findings suggest that targeting methionine deprivation could be a promising approach for the clinical treatment of glioma.