Abstract
Circular RNAs (circRNAs) have recently been reported to play crucial roles in various regulatory processes and involved in cancer onset and progression. However, the potential mechanism of circRNAs in chronic lymphocytic leukemia (CLL) remains largely unknown. Here, we observed hsa_circ_0132266 (circ_0132266), a circRNA significantly decreased in the peripheral blood mononuclear cells (PBMCs) of CLL patients compared with healthy donors, could act as an endogenous sponge of hsa-miR-337-3p (miR-337-3p) and regulate its activity, which resulted in a downstream change of target-gene PML and a consequent influence on cell viability. Taken together, our data indicated the regulatory mechanism of circ_0132266 in CLL progression through circ_0132266/miR-337-3p/PML axis, suggesting that it may serve as a biomarker as well as an exploitable therapeutic target for CLL.
Highlights
Chronic lymphocytic leukemia (CLL), a heterogeneous disease characterized by the monoclonal expansion of B cells, is the commonest leukemia in the western hemisphere [1, 2]
The upregulated miR-92a-3p in CLL patients predicts a favorable prognostic outcome [8]. miR-125a-5p and miR-34a-5p are considered as promising indicators of CLL Richter syndrome transformation [9]. miR-34a is revealed to participate in B-cell receptor (BCR) signaling and affects CLL patients’ treatment [10]
Contrary to these previous reports, in our research, we accidentally found that miR-337-3p exhibited obviously high expression in peripheral blood mononuclear cell (PBMCs) of CLL patients compared with normal controls
Summary
Chronic lymphocytic leukemia (CLL), a heterogeneous disease characterized by the monoclonal expansion of B cells, is the commonest leukemia in the western hemisphere [1, 2]. MiR-337-3p which has been detected to be downregulated in clear cell renal cell carcinoma [11], gastric cancer [12] and hepatocellular carcinoma [13, 14], could function as a suppressive factor in cell proliferation, tumor growth and metastasis through directly regulating target genes. Contrary to these previous reports, in our research, we accidentally found that miR-337-3p exhibited obviously high expression in peripheral blood mononuclear cell (PBMCs) of CLL patients compared with normal controls. The current results inspired us to further explore its regulatory mechanism
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