Ying Yu#, Shuni Zhou#, Li Hou*
Department of Cardiovascular Diseases, The National Hospital of Enshi Autonomous Prefecture, Enshi 445000, Hubei province, China
Objective: To explore the role of lncRNA-XIST (XIST) in promoting cell apoptosis in patients with chronic heart failure (CHF) by regulating miR-126.
Methods: A total of 114 CHF patients treated in our hospital were enrolled as a research group, and 92 healthy people in physical examination during the same period were enrolled as a control group. Myocardial cell were purchased. A polymerase chain reaction (PCR) assay was conducted to quantify XIST and miR-126 in the cells of CHF patients, and the correlation of XIST expression with clinicopathological features and prognosis of the research subjects was analyzed. The influences of XIST on the biological functions of CHF cells were also analyzed, and the regulatory relationbetween XIST and miR-126 in CHF cells was studied.
Results: XIST was over-expressed in the serum of CHF patients, while miR-126 was lowly expressed in it, and the expression of the two was negatively correlated. Multivariate Cox analysis revealed that high XIST expression, age, renal insufficiency, smoking history, and New York Heart Association classification were independent factors for prognosis of CHF patients. Overexpression of miR-126 and silence of XIST suppressed invasion and proliferation of CHF cells, and promoted apoptosis of them. Moreover, co-transfection of XIST-inhibitor + miR-126-mimics inhibited the invasion and proliferation of AC19 more significantly and strengthened the apoptosis of them more strongly. Furthermore, inhibition of XIST could increase the expression of miR-126, thus weakening the invasion and proliferation of CHF cells and strengthening their apoptosis.
Conclusion: Inhibition of XIST can weaken the proliferation and invasion of CHF cells and strengthen the apoptosis of them by up-regulating miR-126.
XIST, miR-126, chronic heart failure, biological function.
10.19193/0393-6384_2021_6_547