Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Homeobox transcript antisense intergenic RNA (HOTAIR), as a long non-coding RNA (lncRNA), has been considered to play critical roles in the biological properties of various tumors. The purposes of this study were to investigate the role and possible molecular mechanisms of HOTAIR in regulating the permeability of blood tumor barrier (BTB) in vitro. Our present study elucidated that the expressions of HOTAIR and upstream stimulatory factor 1 (USF1) was up-regulated, but miR-148b-3p was down-regulated in glioma microvascular endothelial cells (GECs). Knockdown of HOTAIR could increase the permeability of BTB as well as down-regulated the expressions of tight junction related proteins ZO-1, occludin, claudin-5, but up-regulated miR-148b-3p expressions in GECs. Meanwhile, dual-luciferase reporter assays demonstrated that HOTAIR was a target RNA of miR-148b-3p. Furthermore, overexpression of miR-148b-3p increased the permeability of BTB by down-regulating the expressions of tight junction related proteins and USF1 in GECs, and vice versa. And further result revealed USF1 was a target of miR-148b-3p. Silence of USF1 increased the permeability of BTB duo to their interaction with the promoters of ZO-1, occludin, and claudin-5 in GECs. Taken together, our finding indicated that knockdown of HOTAIR increased BTB permeability via binding to miR-148b-3p, which further reducing tight junction related proteins in GECs by targeting USF1. Thus, HOTAIR will attract more attention since it can serve as a potential target of drug delivery across BTB and may provide novel strategies for glioma treatment.
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PMID:The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB. 2870 16

Circular RNAs (circRNAs) play important roles in the development and treatment of glioma. However, the role and mechanism of circRNA carboxypeptidase A4 (circ0082374) in glioma are largely unknown. Forty-two glioma patients and 28 normal patients were recruited. Glioma cell lines A172 and U251 were used for functional assays. The expression levels of circ0082374, microRNA-326 (miR-326) and sirtuin 1 (SIRT1) were examined via quantitative real-time polymerase chain reaction or western blot. Cell viability, migration, invasion and glycolysis were measured via cell counting kit-8, trans-well, oxygen consumption rate and western blot, respectively. The target correlation of circ0082374/miR-326 or miR-326/SIRT1 was explored via dual-luciferase reporter, RNA immunoprecipitation and pull-down assays. The role of circ0082374 in vivo was investigated via xenograft model. We found circ0082374 expression was elevated in glioma tissues and cells. Knockdown of circ0082374 suppressed the viability, migration, invasion and glycolysis in glioma cells. miR-326 was a target of circ0082374 and miR-326 knockdown attenuated the inhibitive role of circ0082374 silence in glioma progression. SIRT1 was a target of miR-326 and circ0082374 could promote SIRT1 expression by sponging miR-326. Silence of SIRT1 reversed the promoting effect of circ0082374 on glioma progression. Knockdown of circ0082374 reduced xenograft tumor growth by miR-326/SIRT1 in vivo. Collectively, silence of circ0082374 repressed the viability, migration, invasion and glycolysis in glioma cells by regulating miR-326 and SIRT1 in a ceRNA mechanism, providing a new mechanism for the pathogenesis of glioma.
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PMID:Knockdown of circ0082374 inhibits cell viability, migration, invasion and glycolysis in glioma cells by miR-326/SIRT1. 3289 23