Wangsheng Chen1, Lan Hong2, Changlong Hou3, Genlin Zong3, Jianhua Zhang3. 1. Department of Radiology, Hainan General Hospital, Hainan Hospital of Hainan Medical University Haikou 570311, China. 2. Department of Gynecology, Hainan General Hospital/Hainan Hospital of Hainan Medical University Haikou 570311, China. 3. Department of Radiology, Shanghai East Hospital, Tongji University School of Medicine Shanghai 200120, China.
Abstract
BACKGROUND: LncRNA LINC00665 partakes in controlling the malignant phenotype of cancer cells, but its role in glioma and the related regulatory mechanism remain uncertain. METHODS: RT-PCR was exploited to examine LINC00665 expression. The relationships among the LINC00665 expression, the clinicopathologic values and magnetic resonance imaging (MRI) characteristics of glioma were analyzed. The multiplication, movement, and aggressiveness of glioma cell lines were evaluated by CCK-8, EdU, and Transwell experiments after constructing LINC00665 overexpression and LINC00665 knockdown cell models. A dual-luciferase reporter gene experiment and RIP experiment were executed to validate the interactions between LINC00665 and miR-129-5p, and between miR-129-5p and HMGB1. Western blot and RT-PCR were conducted to find the impact of LINC00665 and miR-129-5p on HMGB1 expression. Nude mouse model was also constructed to examine the impact of LINC00665 on multiplication and aggressiveness of glioma cells in vivo. RESULTS: LINC00665 expression was markedly increased in glioma. High LINC00665 expression in glioma was closely linked to larger tumor diameter, higher pathologic grade, heterogeneous MRI signal of the tumor, increased peritumoral edema, and stronger MRI enhancement characteristics. LINC00665 overexpression facilitated the malignant behavior of glioma cells, while LINC00665 knockdown played the reverse role. Mechanistically, LINC00665 could decoy miR-129-5p, and indirectly increased HMGB1 expression. CONCLUSION: LINC00665 functions as an oncogenic lncRNA in glioma, to accelerate glioma progression by modulating miR-129-5p and increasing HMGB1 expression. AJTR
BACKGROUND: LncRNA LINC00665 partakes in controlling the malignant phenotype of cancer cells, but its role in glioma and the related regulatory mechanism remain uncertain. METHODS: RT-PCR was exploited to examine LINC00665 expression. The relationships among the LINC00665 expression, the clinicopathologic values and magnetic resonance imaging (MRI) characteristics of glioma were analyzed. The multiplication, movement, and aggressiveness of glioma cell lines were evaluated by CCK-8, EdU, and Transwell experiments after constructing LINC00665 overexpression and LINC00665 knockdown cell models. A dual-luciferase reporter gene experiment and RIP experiment were executed to validate the interactions between LINC00665 and miR-129-5p, and between miR-129-5p and HMGB1. Western blot and RT-PCR were conducted to find the impact of LINC00665 and miR-129-5p on HMGB1 expression. Nude mouse model was also constructed to examine the impact of LINC00665 on multiplication and aggressiveness of glioma cells in vivo. RESULTS: LINC00665 expression was markedly increased in glioma. High LINC00665 expression in glioma was closely linked to larger tumor diameter, higher pathologic grade, heterogeneous MRI signal of the tumor, increased peritumoral edema, and stronger MRI enhancement characteristics. LINC00665 overexpression facilitated the malignant behavior of glioma cells, while LINC00665 knockdown played the reverse role. Mechanistically, LINC00665 could decoy miR-129-5p, and indirectly increased HMGB1 expression. CONCLUSION: LINC00665 functions as an oncogenic lncRNA in glioma, to accelerate glioma progression by modulating miR-129-5p and increasing HMGB1 expression. AJTR