The effect of miR-146a on STAT1 expression and apoptosis in acute lymphoblastic leukemia Jurkat cells

• Published in: Oncology letters Vol. 13; no. 1; pp. 151 - 154
• Main Authors: Yan, Weihong, Guo, Hua, Suo, Feng, Han, Chunling, Zheng, Hua, Chen, Tong
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.01.2017; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: acute lymphoblastic leukemia; Acute lymphocytic leukemia; Apoptosis; Care and treatment; Cellulose acetate; Deoxyribonucleic acid; Development and progression; DNA; Gene expression; Genetic aspects; Health aspects; Jurkat cells; Kinases; Leukemia; Membranes; MicroRNA; miR-146a; Oncology; Phosphorylation; Proteins; STAT1; Stem cells; Studies; United States > US; China; Jurkat cells; apoptosis; miR-146a; STAT1; acute lymphoblastic leukemia
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2016.5395

The effect of miR-146a-dependent regulation of STAT1 on apoptosis in acute lymphoblastic leukemia (ALL) Jurkat cells was investigated. The miR-146a mimic and miR-146a inhibitor vectors were constructed in vitro, and experimental grouping was as follows: Control group (untreated Jurkat cells), empty vector group (Jurkat cells transfected with empty vector), agonist group (Jurkat cells transfected with miR-146a mimic) and the inhibitor group (Jurkat cells transfected with miR-146a inhibitor). Western blot analysis was used to observe the expression, respectively, of STAT1, p-STAT1 and Bcl-xL, and flow cytometry was used to test apoptosis in Jurkat cells. STAT1 and p-STAT1 expression in the agonist group was higher than that in the control and empty vector groups, but lower in the inhibitor group, and differences were statistically significant (P<0.05). The rate of apoptosis in the agonist group was significantly higher than that of the control group and blank vector group, and it was significantly lower in the inhibitor group (P<0.05). As a tumor suppressor, miR-146a can regulate expression of apoptosis-promoting factor STAT1, and anti-apoptosis factor Bcl-xL, and is able to promote apoptosis of ALL Jurkat cells.