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MicroRNA-145-3p suppresses the malignant behaviors of T-cell acute lymphoblastic leukemia Jurkat cells via inhibiting the NFkappaB signaling pathway

Xin YANG*, Liqun LU, Li HUANG, Jing HE, Jie LV

Department of Pediatrics, The First Affiliated Hospital of Chengdu Medical College, Chengdu, China

*Address correspondence to: Xin Yang, email

BIOCELL 2020, 44(1), 101-110. https://doi.org/10.32604/biocell.2020.08324

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is a hematological tumor caused by the malignant transformation of immature T-cell progenitor cells. Emerging studies have stated that microRNAs (miRNAs) may play key roles in T-ALL progression. This study aimed to investigate the roles of miR-145-3p in T-ALL cell proliferation, invasion, and apoptosis with the involvement of the nuclear factor-kappaB (NF-κB) signaling pathway. T-ALL Jurkat cells were harvested, and the expression of miR-145-3p and NF-κB-p65 was measured. Gain- and loss-of-functions of miR-145-3p and NF-κB-p65 were performed to identify their roles in the biological behaviors of Jurkat cells, including proliferation, apoptosis, and invasion. Consequently, the current study demonstrated that miR-145-3p was downregulated while NF-κB-p65 was up-regulated in Jurkat cells. miR-145-3p directly bound to the 3’ untranslated region of NF-κB-p65. Over-expression of miR-145-3p inhibited Jurkat cell proliferation, invasion, and resistance to apoptosis, while over-expression of NF-κB-p65 presented opposite trends. Co-transfection of miR-145-3p and NF-κB-p65 promoted the malignant behaviors of Jurkat cells compared to miR-145-3p transfection alone, while it reduced these behaviors of Jurkat cells compared to NF-κB-p65 transfection alone. Taken together, this study provided evidence that miR-145-3p could suppress proliferation, invasion, and resistance to the death of T-ALL cells via inactivating the NF- κB signaling pathway.

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YANG, X., LU,, L. (2020). MicroRNA-145-3p suppresses the malignant behaviors of T-cell acute lymphoblastic leukemia Jurkat cells via inhibiting the NFkappaB signaling pathway. BIOCELL, 44(1), 101–110. https://doi.org/10.32604/biocell.2020.08324



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