Effect of microRNA-153 targeting phosphatidylinositol 3 kinase/serine-threonine protein kinase signaling pathway on proliferation in acute lymphoblastic leukemia cell
Yan Gu, Hongwei Wang, Lei Han
Abstract
Yan Gu, Hongwei Wang, Lei Han
Abstract
Objective To investigate the effect of microRNA (miRNA, miR)-153 on the proliferation and apoptosis of in human acute lymphoblastic leukemia (ALL) cell line Jurkat cells by phosphatidylinositol 3 kinase (PI3K)/serine-threonine protein kinase (Akt) pathway. Methods After miR-153 mimics (miR-153 mimics group) and miR-153 inhibitor (miR-153 inhibitor group) were transfected into Jurkat cells, cell proliferation, cycle and apoptosis. was detected; the expression of miR-153, PI3K and Akt mRNA and protein was measured; whether PI3K was the target gene of miR-153. was confirmed. Results Compared with the negative control group, the expression of miR-153 in the miR-153 mimics group was significantly increased by approximately 10-fold (t=39.596, P<0.01), and the expression of miR-153 was significantly decreased in the miR-153 inhibitor group (t=14.651, P<0.01). The activity of the cells in the miR-153 mimics group was significantly decreased (t=10.931, P<0.01), and the activity of the miR-153 inhibitor group was significantly increased (t=7.640, P<0.01). The expression of PI3K total protein, PI3K mRNA and p-Akt in the miR-153 mimics group was significantly decreased (t=7.161, P<0.01; t=6.684, P<0.01; t=10.769, P<0.01), and the expression of PI3K total protein, PI3K mRNA and p-Akt in the miR-153 inhibitor group was significantly increased (t=3.998, P<0.05; t=8.902, P<0.01; t=7.078, P<0.01). The proportion of G0/G1 phase cells increased significantly, while the S phase and G2/M phasecells decreased significantly (t=3.786, P<0.05; t=3.012, P<0.05; t=4.948, P<0.01) in the miR-153 mimics group; the G0/G1 phase cells decreased significantly, and the proportion of cells in S phase and G2/M phase increased significantly (t=5.356, P<0.01; t=3.055, P<0.05; t=3.893, P<0.05) in the miR-153 inhibitor group. The apoptosis rate of the miR-153 mimics group was significantly increased (t=4.673, P<0.05), while the apoptotic rate of the miR-153 inhibitor group was significant decline (t=5.618, P<0.01). Compared to the empty plasmid group, the relative luciferase activity of 3’untranslated regions (3’UTR) plasmid group was significantly reduced (t=7.925, P<0.01). Conclusion MiR-153 can directly target PI3K/Akt signaling pathway and regulate Jurkat cell proliferation and apoptosis. Key words: Acute lymphoblastic leukemia; MicroRNA-153; Phosphatidylinositol 3 kinase/serine-threonine protein kinase signaling pathway
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the effect of microRNA (miRNA, miR)-153 on the proliferation and apoptosis of in human acute lymphoblastic leukemia (ALL) cell line Jurkat cells by phosphatidylinositol 3 kinase (PI3K)/serine-threonine protein kinase (Akt) pathway. Methods After miR-153 mimics (miR-153 mimics group) and miR-153 inhibitor (miR-153 inhibitor group) were transfected into Jurkat cells, cell proliferation, cycle and apoptosis. was detected; the expression of miR-153, PI3K and Akt mRNA and protein was measured; whether PI3K was the target gene of miR-153. was confirmed. Results Compared with the negative control group, the expression of miR-153 in the miR-153 mimics group was significantly increased by approximately 10-fold (t=39.596, P<0.01), and the expression of miR-153 was significantly decreased in the miR-153 inhibitor group (t=14.651, P<0.01). The activity of the cells in the miR-153 mimics group was significantly decreased (t=10.931, P<0.01), and the activity of the miR-153 inhibitor group was significantly increased (t=7.640, P<0.01). The expression of PI3K total protein, PI3K mRNA and p-Akt in the miR-153 mimics group was significantly decreased (t=7.161, P<0.01; t=6.684, P<0.01; t=10.769, P<0.01), and the expression of PI3K total protein, PI3K mRNA and p-Akt in the miR-153 inhibitor group was significantly increased (t=3.998, P<0.05; t=8.902, P<0.01; t=7.078, P<0.01). The proportion of G0/G1 phase cells increased significantly, while the S phase and G2/M phasecells decreased significantly (t=3.786, P<0.05; t=3.012, P<0.05; t=4.948, P<0.01) in the miR-153 mimics group; the G0/G1 phase cells decreased significantly, and the proportion of cells in S phase and G2/M phase increased significantly (t=5.356, P<0.01; t=3.055, P<0.05; t=3.893, P<0.05) in the miR-153 inhibitor group. The apoptosis rate of the miR-153 mimics group was significantly increased (t=4.673, P<0.05), while the apoptotic rate of the miR-153 inhibitor group was significant decline (t=5.618, P<0.01). Compared to the empty plasmid group, the relative luciferase activity of 3’untranslated regions (3’UTR) plasmid group was significantly reduced (t=7.925, P<0.01). Conclusion MiR-153 can directly target PI3K/Akt signaling pathway and regulate Jurkat cell proliferation and apoptosis. Key words: Acute lymphoblastic leukemia; MicroRNA-153; Phosphatidylinositol 3 kinase/serine-threonine protein kinase signaling pathway
Key concepts: Jurkat cells, Protein kinase B, PI3K/AKT/mTOR pathway, Molecular biology, Phosphatidylinositol, Kinase, Apoptosis, microRNA