Abstract
BackgroundAntisense non-coding RNA in the INK4 locus (ANRIL) is of great importance in cell biological behaviors, and ANRIL functions in many kinds of cancers including leukemia. However, the mechanism of ANRIL in the progression of T-cell acute lymphoblastic leukemia (T-ALL) has not been clarified clearly.MethodsqRT-PCR was performed to detect ANRIL expression in T-ALL samples. T-ALL cell lines (MOLT4, CCRF-CEM and KOPT-K1) were used as the cell models. The function of ANRIL on T-ALL cells was investigated by CCK-8 assays, Transwell assays, and apoptosis experiments in vitro. qRT-PCR, Western blot, luciferase reporter assay and RIP assay were used to confirm the interactions between ANRIL and miR-7-5p, miR-7-5p and its target gene transcription factor 4 (TCF4).ResultsANRIL was significantly up-regulated in T-ALL samples. Its knockdown markedly inhibited viability, migration and invasion of T-ALL cells, but its overexpression exerted the opposite effects. TCF4 was proved to be a target gene of miR-7-5p. ANRIL down-regulated miR-7-5p via sponging it and in turn up-regulated TCF4.ConclusionsLncRNA ANRIL can modulate malignant phenotypes of T-ALL cells, possibly by regulating miR-7-5p/TCF4 axis, and it serves as a potential therapeutic target for T-ALL.
Highlights
Antisense non-coding RNA in the INK4 locus (ANRIL) is of great importance in cell biological behaviors, and ANRIL functions in many kinds of cancers including leukemia
ANRIL and transcription factor 4 (TCF4) were remarkably highly expressed in bone marrow tissues of T‐Acute lymphocytic leukemia (ALL) patients, while miR‐7‐5p was significantly lowly expressed To explore the associations among ANRIL, miR-7-5p and TCF4, we firstly used qRT-PCR to detect ANRIL, miR7-5p and TCF4 mRNA expressions respectively in bone marrow tissues of patients with T-cell acute lymphoblastic leukemia (T-ALL) and healthy volunteers
The results suggested that compared with that of healthy controls, the expressions of ANRIL and TCF4 in bone marrow tissue of T-ALL patients were dramatically up-regulated, while miR-7-5p expression was downregulated (P < 0.001, Fig. 1 a–c)
Summary
Antisense non-coding RNA in the INK4 locus (ANRIL) is of great importance in cell biological behaviors, and ANRIL functions in many kinds of cancers including leukemia. The mechanism of ANRIL in the progression of T-cell acute lymphoblastic leukemia (T-ALL) has not been clarified clearly. LncRNAs can work as oncogenes or tumor suppressors in various tumors, and their abnormal expression levels can be used as indicators for tumor occurrence, metastasis or recurrence [11, 12]. An enormous number of studies authenticate that the dysregulation of antisense non-coding RNA in the INK4 locus (ANRIL) is related to the progression of multiple cancers [13,14,15,16,17]. ANRIL promotes tumorigenesis through up-regulation of EGFR1 expression in
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