The lncRNA SLCO4A1‐AS1/miR‐876‐3p/RBBP6 axis regulates cell proliferation and apoptosis in acute lymphocytic leukemia via the JNK signaling pathway.

Introduction: Acute lymphocytic leukemia (ALL) is a hematologic malignancy caused by the clonal proliferation of immature lymphocytes. Long noncoding RNAs (lncRNAs) have been reported as critical regulators in several cancers, including ALL. LncRNA SLCO4A1 antisense RNA 1 (SLCO4A1‐AS1) has been revealed to be implicated in tumorigenesis of several cancers. Our study focused on the role of SLCO4A1‐AS1 in ALL. Methods: RT‐qPCR, Western blot analysis, CCK‐8, EdU, and Flow cytometry analysis were used to explore the biological function of SLCO4A1‐AS1 in ALL cellular processes. Luciferase reporter and RNA pull‐down assays were applied to explore the mechanism of SLCO4A1‐AS1 in ALL cells. Results: SLCO4A1‐AS1 was upregulated in ALL tissues and cell lines. We found that suppression of SLCO4A1‐AS1 suppressed ALL cell proliferation and facilitated cell apoptosis. Our result confirmed that SLCO4A1‐AS1 acted as a ceRNA by sponging microRNA 876‐3p (miR‐876‐3p) to upregulate retinoblastoma binding protein 6 (RBBP6) expression in ALL cells. Moreover, SLCO4A1‐AS1 activated the JNK signaling pathway by upregulating RBBP6. Rescue assays revealed that the activation of the JNK signaling or overexpression of RBBP6 revered the suppressive effect of SLCO4A1‐AS1 knockdown on growth of ALL cells. Conclusion: SLCO4A1‐AS1 promoted cell growth of ALL by the miR‐876‐3p/RBBP6 axis to activate the JNK signaling pathway. [ABSTRACT FROM AUTHOR]