Studies shown that its overexpression induces apoptosis and inhibits cell growth in U118 and U87 glioma cells by downregulating BRE gene expression, which influences the levels of p53, CDK2, and Cyclin A proteins, while elevated HOTTIP levels in temozolomide-resistant glioma cell lines A172, LN229, and SF268 enhance proliferation, migration, clonogenicity, and markers of angiogenesis and metastasis, highlighting its potential as therapeutic target [88,89]. This evidence concerns the gene TP53 and central nervous system cancer.