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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Hematol+Oncol
2018 ; 11
(1
): 77
Nephropedia Template TP
gab.com Text
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A cytoplasmic long noncoding RNA LINC00470 as a new AKT activator to mediate
glioblastoma cell autophagy
#MMPMID29866190
Liu C
; Zhang Y
; She X
; Fan L
; Li P
; Feng J
; Fu H
; Liu Q
; Liu Q
; Zhao C
; Sun Y
; Wu M
J Hematol Oncol
2018[Jun]; 11
(1
): 77
PMID29866190
show ga
BACKGROUND: Despite the overwhelming number of investigations on AKT, little is
known about lncRNA on AKT regulation, especially in GBM cells. METHODS:
RNA-binding protein immunoprecipitation assay (RIP) and RNA pulldown were used to
confirm the binding of LINC00470 and fused in sarcoma (FUS). Confocal imaging,
co-immunoprecipitation (Co-IP) and GST pulldown assays were used to detect the
interaction between FUS and AKT. EdU assay, CCK-8 assay, and intracranial
xenograft assays were performed to demonstrate the effect of LINC00470 on the
malignant phenotype of GBM cells. RT-qPCR and Western blotting were performed to
test the effect of LINC00470 on AKT and pAKT. RESULTS: In this study, we
demonstrated that LINC00470 was a positive regulator for AKT activation in GBM.
LINC00470 bound to FUS and AKT to form a ternary complex, anchoring FUS in the
cytoplasm to increase AKT activity. Higher pAKT activated by LINC00470 inhibited
ubiquitination of HK1, which affected glycolysis, and inhibited cell autophagy.
Furthermore, higher LINC00470 expression was associated with GBM tumorigenesis
and poor patient prognosis. CONCLUSIONS: Our findings revealed a noncanonical AKT
activation signaling pathway, i.e., LINC00470 directly interacts with FUS,
serving as an AKT activator to promote GBM progression. LINC00470 has an
important referential significance to evaluate the prognosis of patients.
|*Autophagy
[MESH]
|Cell Line, Tumor
[MESH]
|Cytoplasm/genetics/metabolism
[MESH]
|Disease Progression
[MESH]
|Glioblastoma/*pathology
[MESH]
|Humans
[MESH]
|Prognosis
[MESH]
|Protein Binding
[MESH]
|Proto-Oncogene Proteins c-akt/*metabolism
[MESH]
|RNA, Long Noncoding/*physiology
[MESH]
|RNA-Binding Protein FUS/metabolism/physiology
[MESH]