Multifaceted Cooperation Between WNT and PI3K Signaling Axis through the Long Noncoding RNA SNHG16 and TCF7 in de novo Acute Lymphoblastic Leukemia Patients

Authors
Mohadeseh Khani 1
Atbin Latifi 2
Mohammad Sayyadi 3
1 Arak University of Medical Sciences, Arak, Iran
2 Department of Internal Medicine, School of Medical Sciences, Arak University of Medical Sciences, Arak, Iran
3 Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Arak University of Medical Sciences, Arak, Iran
10.61882/ibj.5031
Abstract
Background: Acute lymphoblastic leukemia (ALL) is the most prevalent form of acute leukemia in children, arising from the known and unknown factors. This complexity has limited advancements in patient recovery. Recently, long noncoding RNAs lncRNA (lncRNA) molecules have emerged as significant but not fully understood players in leukemia research. Studies have indicated that c-Myc can stimulate and enhance gene expression through multiple pathways, particularly by activating the PI3K and WNT pathways. The present study investigated the expression levels of lncRNAs involved in the upstream regulation of the PI3K/WNT pathways in patients diagnosed with ALL.

Methods: This case-control cross-sectional study was conducted using RNA from blood samples. The study examined 36 patients with ALL and 36 healthy controls. The expression levels of SNHG16 and TCF7 lncRNAs and their target genes were determined using qRT-PCR.

Results: The expression of Akt, β-catenin and c-Myc genes in the patient group showed a significant increase compared to the control group (p < 0.05). The expression levels of SNHG16 and TCF7 were significantly elevated in ALL patients compared to the control group (p < 0.05). Furthermore, a significant positive correlation was observed between the expression levels of these two lncRNAs in the patient group (p < 0.05).

Conclusion: Our findings demonstrate that SNHG16 and TCF7 lncRNA may act as crucial regulators of the Akt and β-catenin in ALL, which in turn influence c-Myc expression levels in affected individuals. Further research is needed to better understand the molecular mechanisms underlying ALL, potentially leading to improved treatment and monitoring strategies for patients.
Keywords
SNHG16 lncRNA
TCF7
WNT Signaling Pathway