MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR / 中国肺癌杂志

BACKGROUND@#Non-small cell lung cancer (NSCLC) is a kind of lung cancer, because its high incidence has been concerned. Therefore, it has great significance to reveal the pathogenesis of NSCLC. As a transcriptional regulatory factor, MATF-A plays an important role in the development of multiple tumors, can regulate the migration process of a variety of tumor cells. HOTAIR is a long non-coding RNA (LncRNA) found in recent years, which expresses abnormally in multiple tumors and is involved in the proliferation and migration of multiple tumors. The aim of this study is to explore the role of MRTF-A through HOTAIR to regulate the proliferation and migration of NSCLC cell A549 cell.@*METHODS@#We constructed the overexpression plasmid and interfering plasmid of MRTF-A, and detected the effect of MRTF-A on the proliferation and migration of A549 cells by CCK8 and wound healing methods respectively. Then, we designed the siRNA of HOTAIR to detect its effect on the proliferation and migration of A549 cells. Through qRT-PCR, we detected the effect of MRTF-A on HOTAIR expression. Finally, we constructed HOTAIR's promoter, and detect the effect of MRTF-A on HOTAIR promoter activity by luciferase reporter gene test.@*RESULTS@#Overexpression of MRTF-A promotes the proliferation and migration of A549 cells, while silent MRTF-A inhibits its proliferation and migration. Next, we found that interfered HOTAIR expression inhibited the proliferation of A549 cells. We found that MRTF-A could influence the expression of HOTAIR and regulate the activity of HOTAIR promoter.@*CONCLUSIONS@#MRTF-A regulates the proliferation and migration of A549 cell through HOTAIR.

MRTF-A alleviates myocardial ischemia reperfusion injury via inhibiting TLR4/TRIF signaling pathways / 中华急诊医学杂志

Objective To observe the effect of myocardial transcription factor MRTF-A on myocardium inflammation and its mechanism.Methods Totally 30 rats were randomly divided into the sham,ischemia-reperfusion (myocardial ischemia 30 min and reperfusion 2 h),and MRTF-A groups(myocardial ischemia 30 min and reperfusion 2 h & Lentivirus infection MRTF-A) (n=10 each group).Serum myocardial enzyme activity was detected by biochemical analysis,myocardial infarct size detected by TTC,and degree of myocardial injury was measured by HE staining.The TLR4 and TRIF expression was analyzed by immunohistochemistry and qPCR.Results Compared with the sham group,the MRTF-A group significantly increased the activity of serum myocardial enzymes CK-MB and LDH (P＜0.05).The infarct area of myocardial tissue was gray-white,and the infarct area was (54.31±3.07)％ (P ＜ 0.05).Myocardial fibrosis was disorder,myocardial cell was swollen and burst,and inflammatory cell infiltration was obvious.Protein and mRNA expressions of TRL4 and TRIF were significantly up-regulated (P＜0.05).Compared with the ischemia-reperfusion group,the levels of CK-MB and LDH were significantly reduced after myocardial infection with MRTF-A (P＜0.05).The myocardial infarction area was significantly reduced to (16.74±4.26)％ (P＜ 0.05).The myocardial structure was nearly normal with mild edema.Protein and mRNA expression of TRL4 and TRIF decreased significantly (P＜0.05).Conclusions The overexpression of transcription factor MRTF-A in myocardial cells alleviates the myocardial ischemia reperfusion injury by inhibiting the TLR4/TRIF signaling pathway and reducing the serum myocardial enzyme activity and myocardial damage.

MRTF-A mediates FN and ICAM-1expressions by NF-κB pathway in AGEs-induced GMCs / 中国药理学通报

Aim To observe the expression of MRTF-A in rat glomerular mesangial cells(GMCs) induced by advanced glycation end products(AGEs) and its effect on ICAM-1 and FN;to explore whether MRTF-A is involved in the process of diabetic nephropathy by affecting NF-κB pathway.Methods Under the condition of AGEs, CCG-1423 and anti-MRTF-A small interfering RNA were used to knock down MRTF-A and MRTF-A plasmid was used to activatt MRTF-A, The expression level of MRTF-A, ICAM-1, FN and p65 in nucleus were detected by Western blot.Results The protein expressions of MRTF-A was increased in AGEs-induced GMCs.The expressions of FN and ICAM-1 and p65 in nucleus were downregulated by knocking down MRTF-A.However, the expressions of FN, ICAM-1 and p65 in nucleus were upregulated by overexpressing MRTF-A.Conclusions AGEs can upregulate the expression of MRTF-A in GMCs, and MRTF-A mediates the protein expressions of FN and ICAM-1 by affecting NF-κB signaling pathway in AGEs-induced GMCs.