RESUMO
The metastasis-associated lung adenocarcinoma transcription 1 (MALAT1) is a highly conserved long non-coding RNA (lncRNA) gene. However, little is known about the pathological role of lncRNA MALAT1 in glioma. In the present study, we explored the expression level of lncRNA MALAT1 in primary glioma tissues as well as in U87 and U251 glioma cell lines. Using qRT-PCR, we found that the expression of lncRNA MALAT1 was significantly increased in glioma tissues compared with that of paracancerous tissues. Meanwhile, the expression of MALAT1 was highly expressed in U98 and U251 cells. In order to explore the function of MALAT1, the expression of MALAT1 was greatly reduced in U87 and U251 cells transfected with siRNA specifically targeting MALAT1. Consequently, cell viability of U87 and U251 cells were drastically decreased after the knockdown of MALAT1. Concomitantly, the apoptosis rate of the two cell lines was dramatically increased. Furthermore, the expression levels of some tumor markers were reduced after the knockdown of MALAT1, such as CCND1 and MYC. In summary, the current study indicated a promoting role of MALAT1 in the development of glioma cell.
Assuntos
Humanos , Apoptose , Biomarcadores Tumorais/genética , Western Blotting , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Ciclina D1/genética , Regulação para Baixo , Citometria de Fluxo , Glioma/metabolismo , Proteínas Proto-Oncogênicas c-myc/genética , Interferência de RNA , RNA Longo não Codificante/antagonistas & inibidores , RNA Interferente Pequeno/metabolismo , Reação em Cadeia da Polimerase em Tempo RealRESUMO
Objectives:To compare the susceptibility of serum lipoproteins to oxidation and the effects of high-density lipoprotein on oxidative stress in patients with lipid turbulence. Methods:VLDL, LDL and HDL were isolated using sequential ultracentrifugation from serum of patients with chronic renal failure (CRF) (n=45), myocardial infarction survivor (MIS) (n=33) , cerebral infarction(CI)(n=33) ,type 2 diabetes mellitus(DM)(n=53) and normal individuals (n=44). The degree of lipid peroxidation was estimated using the thiobarbituric acid-reactive substances (TBARS) value and the susceptibilities of lipoproteins to oxidation were assessed by measuring the increased absorbance value at 234 nm due to the conjugated dinene formation. Lipid levels and lipoprotein fractions were measured using standard methods. Results: VLDL obtained from the patient groups showed significant increase in TBARS values, especially from the patients with MIS (compared with control group, P<0.001). In addition, LDL from MIS and DM groups and HDL from CI and DM groups also showed markedly increase in TBARS content. Significant decrease in lag time was observed in both VLDL and LDL fractions from the four patient groups. However, no change was found in the lag time in HDL fraction from the patient group compared with control group. In addition, HDL from the four patients exhibited significantly decreased inhibitory effects on in vitro oxidation of LDL, with the most significant decrease in HDL from CRF and MIS groups. Conclusions:The oxidative modification of lipoproteins in vivo in patients with serum lipid turbulence might be involved in the development of atherosclerosis in these patients.