Human gliomas are a heterogeneous group of primary malignant brain tumors, which most commonly occur in central nervous system of both children and adults [
1]. Glioblastoma multiforme (GBM), the most aggressive form of glioma, exhibits advanced features of malignancy, such as rapid tumor cell proliferation, intense apoptosis resistance, florid necrosis, and robust angiogenesis [
2]. The tumor properties underlie the poor clinical outcome by conferring strong resistance to chemotherapy and radiotherapy, and by promoting a neurologically debilitating course leading to death within 12–18 months post diagnosis [
3].
TRIM8 maps to chromosome 10q24.3, a region showing frequent deletion and loss of heterozygosity in human glioma [
4]. TRIM8 encodes a member of the tripartite-motif-containing (TRIM) protein super family involved in a broad range of biological processes, including carcinogenesis [
5]. TRIM8 interacts with and negatively regulates PIAS3, a protein inhibitor of IL-6-dependent activation of STAT3, a signaling pathway important for cancer development and progression [
6]. In agreement with previously data, we recently reported TRIM8 as a new modulator of the p53-mediated tumor suppression mechanism [
7]. Under stress conditions, such as UV exposure, we showed that p53 induces the expression of TRIM8, which in turn stabilizes p53 leading to cell cycle arrest and reduction of cell proliferation through enhancement of p21 and GADD45 expression [
7]. Experimental evidence has outlined
TRIM8 as one of the genes which low expression level correlates with nodal metastatic progression in primary larynx squamous cell carcinoma and whose expression inhibits tumor cell colony formation
in vitro [
8]. Finally, TRIM8 deficit has been showed to impair p53-mediated cellular responses to chemotherapeutic drugs in a model of Renal Cell Carcinoma [
9]. Up regulation of
miR-17, associated with advanced tumor progression and poor overall survival of gliomas [
10], has been shown to reduce the levels of
TRIM8 in primary chronic lymphocytic leukemia cells, although a direct regulation was not yet demonstrated [
11].