Lentivirus-mediated silencing of HSDL2 suppresses cell proliferation in human gliomas.

Abstract

Gliomas are the most common type of malignant brain tumors, and the related prognosis is poor. Though many genes have been identified as factors in the development and progression of gliomas, underlying mechanisms remained unclear. It was clear that abnormal lipid metabolism was one of the major hallmarks of cancers. However, few factors associated with lipid metabolism have been reported to be involved in cancer pathogenesis. Hydroxysteroid dehydrogenase-like 2 (HSDL2) is a protein containing sterol carrier protein 2 (SCP2) domain localized in peroxisomes, which indicated that HSDL2 might be a fatty acid regulatory factor. Here, we revealed that HSDL2 was significantly upregulated in gliomas and its expression was positively correlated with glioma grades. Furthermore, lentiviral-mediated HSDL2 knockdown showed that HSDL2 downregulation inhibited the proliferation in two human glioblastoma cell lines U-251 cells and U87 MG cells, induced cell cycle arrest, and promoted cell apoptosis. Our study provided multiple lines of evidence for the causal relationship between HSDL2 overexpression and glioma progression and provided possible mechanisms underlying HSDL2-mediated glioma growth. Taken together, these results indicated that HSDL2 might serve as a potential target for glioma treatment in the future.