Original Article
LINC00052 suppressed glioma cell proliferation and invasion by downregulating insulin-like growth factor 2
Abstract
Background: Recent studies have discovered a subtype of noncoding RNAs, long noncoding RNAs (lncRNAs), which are dysregulated in various tumors and associated with carcinogenesis. This study aims to identify the role of lncRNA LINC00052 in glioma tumorigenesis.
Methods: LINC00052 expression was monitored in glioma samples and glioma cells through RT-qPCR. Besides, proliferation assay, transwell assay and wound healing assay were performed to uncover the role of LINC00052 in glioma. Furthermore, the interaction between LINC00052 and insulin-like growth factor 2 (IGF2) in glioma was studied through RT-qPCR and western blot assay.
Results: LINC00052 expression was remarkably downregulated in glioma samples compared with that in normal brain samples. Moreover, cell proliferation, cell invasion and cell migration in glioma were inhibited after overexpression of LINC00052 in vitro. Moreover, after overexpression of LINC00052, IGF2 was downregulated at mRNA and protein level in vitro. Besides, the expression of IGF2 in tumor tissues was negatively correlated to the expression of LINC00052.
Conclusions: These results above suggest that LINC00052 could repress cell migration, invasion and proliferation in glioma through downregulating IGF2, which may offer a new therapeutic intervention for glioma patients.
Methods: LINC00052 expression was monitored in glioma samples and glioma cells through RT-qPCR. Besides, proliferation assay, transwell assay and wound healing assay were performed to uncover the role of LINC00052 in glioma. Furthermore, the interaction between LINC00052 and insulin-like growth factor 2 (IGF2) in glioma was studied through RT-qPCR and western blot assay.
Results: LINC00052 expression was remarkably downregulated in glioma samples compared with that in normal brain samples. Moreover, cell proliferation, cell invasion and cell migration in glioma were inhibited after overexpression of LINC00052 in vitro. Moreover, after overexpression of LINC00052, IGF2 was downregulated at mRNA and protein level in vitro. Besides, the expression of IGF2 in tumor tissues was negatively correlated to the expression of LINC00052.
Conclusions: These results above suggest that LINC00052 could repress cell migration, invasion and proliferation in glioma through downregulating IGF2, which may offer a new therapeutic intervention for glioma patients.
