MicroRNA-124 regulates apoptosis in sevoflurane anesthesia-induced neuroblastoma cells by targeting enhancer of zeste homolog 2

نویسندگان

چکیده

Purpose: To investigate the mechanism of microRNA-124 action on neuroblastoma apoptosis induced by sevoflurane.
 Methods: MiR-124 expression was assessed in a cell line (SMS-KAN) using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The role miR-124 sevoflurane anesthesia-induced studied activity and analysis 3-(4, 5-dimethylthiazolyl-2-yl)-2-5 diphenyl tetrazolium bromide (MTT) assay flow cytometry, respectively. target protein genes were confirmed via luciferase reporter activity, qRT-PCR, western blot analysis.
 Results: upregulated (p < 0.05). After knockdown, significantly reduced viability enhanced SMS-KAN nerve cells Furthermore, significant reduction observed 293T co-transfected with mimics EZH2-wild type (EZH2-WT) mRNA levels EZH2 decreased transfected Overexpression inhibited SMSKAN inhibitor offset siEZH2.
 Conclusion: results suggest that overexpression suppresses proliferation targeting cells. Therefore, represents potential for therapy

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

MicroRNA-137 acts as a tumor suppressor in osteosarcoma by targeting enhancer of zeste homolog 2

MicroRNA (miR) are short non-coding RNA that bind to the 3'-untranslational region of their target genes, inhibiting translation and causing mRNA degradation. miR deregulation has been implicated in human cancer; however, the detailed regulatory mechanism of miR-137 in osteosarcoma (OS) remains largely unknown. In the present study, miR-137 and enhancer of zeste homologue 2 (EZH2) mRNA and prot...

متن کامل

MicroRNA‐124‐3p regulates cell proliferation, invasion, apoptosis, and bioenergetics by targeting PIM1 in astrocytoma

The PIM1 protein is an important regulator of cell proliferation, the cell cycle, apoptosis, and metabolism in various human cancers. MicroRNAs (miRNAs) are powerful post-transcriptional gene regulators that function through translational repression or transcript destabilization. Therefore, we aimed to identify whether a close relationship exists between PIM1 and miRNAs. PIM1 protein levels and...

متن کامل

MicroRNA-205 inhibits renal cells apoptosis via targeting CMTM4

Objective(s):MicroRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression. They have important roles in kidney development, homeostasis and disease, and participate in the onset and progression of tubulointerstitial sclerosis and end-stage glomerular lesions that occur in various forms of chronic kidney disease (CKD). In the present study, we elucidated the role of microR...

متن کامل

MicroRNA-26a suppresses epithelial-mesenchymal transition in human hepatocellular carcinoma by repressing enhancer of zeste homolog 2.

BACKGROUND Our previous study reported that microRNA-26a (miR-26a) inhibited tumor progression by inhibiting tumor angiogenesis and intratumoral macrophage infiltration in hepatocellular carcinoma (HCC). The direct roles of miR-26a on tumor cell invasion remain poorly understood. In this study, we aim to explore the mechanism of miR-26a in modulating epithelial-mesenchymal transition (EMT) in H...

متن کامل

MicroRNA-1 regulates cardiomyocyte apoptosis by targeting Bcl-2.

MicroRNA-1 (miR-1) is preferentially expressed in cardiac muscles, and the expression has been demonstrated to be involved in cardiac development and cardiovascular diseases. Here we report that miR-1 is closely related with ischemia/reperfusion injury in a rat model. The level of miR-1 is inversely correlated with Bcl-2 protein expression in cardiomyocytes of the I/R rat model. In vitro, the l...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Tropical Journal of Pharmaceutical Research

سال: 2021

ISSN: ['1596-5996', '1596-9827']

DOI: https://doi.org/10.4314/tjpr.v18i3.7