A novel lncRNA‐LINC01116 regulates tumorigenesis of glioma by targeting VEGFA

Abstract

Brain glioma is the most common malignant tumor of the central nervous system, and one of the leading causes of death in patients with intracranial tumors. The clinical outcome of glioma is usually poor due to abundant vascularity, fast growth and susceptibility of invasion to normal brain tissues. Our microarray study showed that lncRNA‐LINC01116 was significantly upregulated in glioma tissues and played an important role in cell proliferation, cycle, migration, invasion and angiogenesis. In addition, vascular endothelial growth factor (VEGFA) may be the major target genes in the downstream of lncRNA‐LINC01116. Dual luciferase assay showed that LINC01116 and VEGFA both contained a miR‐31‐5p binding site, and LINC01116 could regulate the expression of VEGFA through competitive absorption of miR‐31‐5p. RNA immunoprecipitation indicated that LINC01116 and VEGFA were present in the miR‐31‐5p‐RISC complex, and biotinylated miR‐31‐5p pull‐down assay suggested that there was a competitive relationship between LINC01116 and VEGFA to bind with miR‐31‐5p. Collectively, our study has identified a novel lncRNA‐LINC01116 and clarified the role and mechanism of LINC01116 in the tumorigenesis of glioma. LINC01116 may prove to be a potential target for the clinical diagnosis and treatment of glioma.

Knockdown of LINC01116 inhibits cell migration and invasion in head and neck squamous cell carcinoma through epithelial‐mesenchymal transition pathway

“…Three overlapping upregulated lncRNAs and three overlapping downregulated lncRNAs were randomly selected to verify the integrated analysis results. 23 In the current study, this is the first direct detection of the effect of LINC01116 on EMT process. Higher levels of LINC01116 were associated with shorter overall survival time (G; P = .017) and relapse-free survival time (H; P = .14).…”

“…Higher levels of LINC01116 were associated with shorter overall survival time (G; P = .017) and relapse-free survival time (H; P = .14). 23 We interpret that LINC01116 could contribute to promoting EMT process by positively regulating VEGF. *P < .05.…”

<p>LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma</p>

“…In addition, LINC01116 was reported to overexpressed and contributed to the progression of nasopharyngeal carcinoma, gastric cancer, osteosarcoma, glioma, epithelial ovarian cancer and head and neck squamous cell carcinoma. [17][18][19][20][21][22][23] However, there is little knowledge on the role of LINC01116 in NSCLC.…”

“…LINC01116 was found to promote the proliferation and migration of osteosarcoma cells through targeting miR-520a-3p and upregulating IL6R via the Jak-stat signaling pathway, 64 and was reported to promote epithelial ovarian cancer progression through regulating cell apoptosis. 23 In addition, LINC01116 was identified to regulates tumorigenesis of glioma by targeting vascular endothelial growth factor A (VEGFA), 22 and LINC01116 was shown to promote gastric cancer cell invasion and migration by positively interacting with lncRNA CASC11. 20 A recent study showed that LINC01116 contributed to gefitinib resistance in NSCLC cells by regulating IFI44 expression.…”

“…17,18 Previous studies have also demonstrated that LINC01116 promotes the progression of nasopharyngeal carcinoma, gastric cancer, osteosarcoma, glioma and epithelial ovarian cancer. [19][20][21][22][23] Furthermore, a recent study showed LINC01116 contributed to gefitinib resistance in NSCLC through affecting IFI44 expression. 24 However, the involvement of LINC01116 in chemoresistance of LAD remains unknown until now.…”