W-J Wang1, K Sun, F-Y Li, X-B Hui, D Liu, J Liu, X-D Wang. 1. Department of Neurosurgery, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huai'an, China. wxdxa19800@126.com.
Abstract
OBJECTIVE: The aim of this study was to uncover the role of lncRNA HANR in the progression of glioma and the underlying mechanism. PATIENTS AND METHODS: HANR expression level in 36 matched glioma tissues and adjacent non-tumoral tissues was determined by qRT-PCR. The relationship between HANR expression and pathological indexes of the glioma patients was analyzed. The Kaplan-Meier method was introduced to investigate the survival of glioma patients. After the knockdown of HANR, the proliferative, migratory, and invasive changes of U251 and SHG44 cells were determined. Bioinformatics and Dual-Luciferase Reporter Gene Assay were applied to predict and verify the downstream target of HANR, respectively. Furthermore, the rescue experiments were conducted to clarify the role of HANR/miRNA-335 regulatory loop in the progression of glioma. RESULTS: HANR was significantly upregulated in glioma tissues and cell lines. Glioma patients with a high expression level of HANR presented remarkably higher rates of lymphatic metastasis and distant metastasis, as well as worse prognosis. The silence of HANR remarkably attenuated the proliferative, migratory, and invasive capacities of U251 and SHG44 cells. MiRNA-335 was the direct target of HANR and was significantly downregulated in glioma tissues. Meanwhile, the miRNA-335 level was negatively regulated by HANR. In addition, the knockdown of miRNA-335 partially reversed the regulatory effects of HANR on cellular behaviors of glioma. CONCLUSIONS: LncRNA HANR is upregulated in glioma, which is closely correlated with metastasis and poor prognosis of glioma patients. In addition, HANR aggravates the progression of glioma by negatively regulating miRNA-335.
OBJECTIVE: The aim of this study was to uncover the role of lncRNA HANR in the progression of glioma and the underlying mechanism. PATIENTS AND METHODS: HANR expression level in 36 matched glioma tissues and adjacent non-tumoral tissues was determined by qRT-PCR. The relationship between HANR expression and pathological indexes of the gliomapatients was analyzed. The Kaplan-Meier method was introduced to investigate the survival of gliomapatients. After the knockdown of HANR, the proliferative, migratory, and invasive changes of U251 and SHG44 cells were determined. Bioinformatics and Dual-Luciferase Reporter Gene Assay were applied to predict and verify the downstream target of HANR, respectively. Furthermore, the rescue experiments were conducted to clarify the role of HANR/miRNA-335 regulatory loop in the progression of glioma. RESULTS: HANR was significantly upregulated in glioma tissues and cell lines. Gliomapatients with a high expression level of HANR presented remarkably higher rates of lymphatic metastasis and distant metastasis, as well as worse prognosis. The silence of HANR remarkably attenuated the proliferative, migratory, and invasive capacities of U251 and SHG44 cells. MiRNA-335 was the direct target of HANR and was significantly downregulated in glioma tissues. Meanwhile, the miRNA-335 level was negatively regulated by HANR. In addition, the knockdown of miRNA-335 partially reversed the regulatory effects of HANR on cellular behaviors of glioma. CONCLUSIONS: LncRNA HANR is upregulated in glioma, which is closely correlated with metastasis and poor prognosis of gliomapatients. In addition, HANR aggravates the progression of glioma by negatively regulating miRNA-335.