Identification of distinctive long noncoding RNA competitive interactions and a six‐methylated‐gene prognostic signature in acute myeloid leukemia with −5/del(5q) or −7/del(7q)

2019 ◽  
Vol 121 (2) ◽  
pp. 1563-1574 ◽  
Author(s):  
Xuejiao YIN ◽  
Sui Huang ◽  
Aoshuang Xu ◽  
Fengjuan Fan ◽  
Lei Chen ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Long Noncoding Rna ◽  
Myeloid Leukemia ◽  
Noncoding Rna ◽  
Competitive Interactions ◽  
Prognostic Signature ◽  
Acute Myeloid

Long noncoding RNA MIAT promotes the progression of acute myeloid leukemia by negatively regulating miR-495

2019 ◽  
Vol 87 ◽  
pp. 106265 ◽  
Author(s):  
Gaoyan Wang ◽  
Xuerong Li ◽  
Liang Song ◽  
Hua Pan ◽  
Jian Jiang ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Long Noncoding Rna ◽  
Myeloid Leukemia ◽  
Noncoding Rna ◽  
Acute Myeloid

Low Expression of Long Noncoding RNA IRAIN Is Associated with Poor Prognosis in Non-M3 Acute Myeloid Leukemia Patients

2018 ◽  
Vol 22 (5) ◽  
pp. 288-294 ◽  
Author(s):  
Hossein Pashaiefar ◽  
Marzieh Izadifard ◽  
Marjan Yaghmaie ◽  
Maryam Montazeri ◽  
Elahe Gheisari ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Long Noncoding Rna ◽  
Myeloid Leukemia ◽  
Noncoding Rna ◽  
Poor Prognosis ◽  
Low Expression ◽  
Acute Myeloid

Long noncoding RNA GAS6 antisense RNA1 silencing attenuates the tumorigenesis of acute myeloid leukemia cells through targeting microRNA-370-3p/Tetraspanin3 axis

2021 ◽  
pp. 1-13
Author(s):  
Weijuan Lei ◽  
Juliar Lin ◽  
Fang Liu ◽  
Nina Chen
Keyword(s):  
Acute Myeloid Leukemia ◽  
Protein Expression ◽  
Long Noncoding Rna ◽  
Myeloid Leukemia ◽  
Noncoding Rna ◽  
Pediatric Patients ◽  
Migration And Invasion ◽  
Pediatric Aml ◽  
Acute Myeloid

PURPOSE: Acute myeloid leukemia (AML) is a type of hematologic malignancy. This study was attempt to explore the effect of long noncoding RNA GAS6 antisense RNA1 (GAS6-AS1) on pediatric AML and the regulation mechanisms. METHODS: GAS6-AS1, microRNA-370-3p (miR-370-3p), and Tetraspanin3 (TSPAN3) expression in bone marrow (BM) tissues and cells was determined by qRT-PCR. The correlation between GAS6-AS1 and clinicopathological features of pediatric patients with AML was assessed. In vitro, viability and migration and invasion of AML cells were evaluated via MTT and transwell assays, respectively. Interactions among GAS6-AS1, miR-370-3p, and TSPAN3 were revealed by dual-luciferase reporter assays. Western blot was applied to confirm the protein expression of TSPAN3. RESULTS: GAS6-AS1 and TSPAN3 expression was elevated in BM tissues of pediatric patients with AML and AML cells, but miR-370-3p expression was reduced. GAS6-AS1 expression was positively related to French-American-British (FAB) classification in pediatric patients with AML. In vitro, GAS6-AS1 deficiency restrained the viability, migration, and invasion of AML cells. Additionally, GAS6-AS1 mediated miR-370-3p expression indeed and TSPAN3 was identified as a target of miR-370-3p. Furthermore, miR-370-3p overexpression repressed the protein expression of TSPAN3. The feedback experiments demonstrated that miR-370-3p inhibition or TSPAN3 overexpression mitigated the suppressive effect of sh-GAS6-AS1 on the tumorigenesis of AML cells. CONCLUSION: GAS6-AS1 silencing restrained AML cell viability, migration, and invasion by targeting miR-370-3p/TSPAN3 axis, affording a novel therapeutic target for pediatric AML.

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