Upregulation of the long noncoding RNA GJA9‐MYCBP and PVT1 is a potential diagnostic biomarker for acute lymphoblastic leukemia

TL;DR

This study shows that increased levels of two specific long noncoding RNAs may help diagnose acute lymphoblastic leukemia in children.

Contribution

The study identifies GJA9-MYCBP and PVT1 lncRNAs as potential new diagnostic biomarkers for ALL.

Findings

GJA9-MYCBP and PVT1 lncRNAs are significantly upregulated in ALL patient samples.

These lncRNAs show strong diagnostic potential with high statistical significance.

MYC mRNA levels and lncRNA expression are positively correlated in ALL patients.

Abstract

Acute lymphoblastic leukemia (ALL) is the most common type of blood cancer in children. Aberrant expression of long noncoding RNAs (lncRNAs) may set stages for ALL development. LncRNAs are emerging as a novel diagnostic and prognostic biomarker for ALL. Herein, we aimed to evaluate the expression of lncRNA GJA9‐MYCBP and PVT1 in blood samples of ALL and healthy individuals.

As a case–control study, 40 pairs of ALL and healthy individual samples were used. The expression of MYC and each candidate lncRNA was measured using quantitative real‐time PCR. Any possible association between the expression of putative noncoding RNAs and clinicopathological characteristics was also evaluated.

LncRNA GJA9‐MYCBP and PVT1 were significantly upregulated in ALL samples compared with healthy ones. Similarly, mRNA levels of MYC were increased in ALL samples than control ones. Receiver operating characteristic curve analysis indicated a satisfactory diagnostic efficacy (p‐value <.0001), suggesting that lncRNA GJA9‐MYCBP and PVT1 may serve as a diagnostic biomarker for ALL. Linear regression analysis unveiled positive correlations between the expression level of MYC and lncRNA GJA9‐MYCBP and PVT1 in ALL patients (p‐values <.01).

In this study, we provided approval for the clinical diagnostic significance of lncRNA GJA9‐MYCBP and PVT1that their upregulations may be a diagnostic biomarker for ALL.

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