<p>Ropivacaine Inhibits Cell Proliferation, Migration and Invasion, Whereas Induces Oxidative Stress and Cell Apoptosis by circSCAF11/miR-145-5p Axis in Glioma</p>

Abstract

Background Glioma is a heterogeneous aggressive tumor. Ropivacaine, a widely used anesthetic, has been shown to repress the progression of multiple cancers, including glioma. In this study, the effects of ropivacaine on cell proliferation, migration, invasion and apoptosis in glioma were revealed. Methods The expression levels of circSCAF11 and miR-145-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in glioma tissues and cells. The expression levels of epithelial–mesenchymal transition (EMT)-related proteins were determined by Western blot. Oxidative stress was evaluated by the measurement of reactive oxygen species (ROS) and determination of mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) assay in glioma cells. Cell proliferation was determined by cell counting kit-8 (CCK-8) assay and cell colony formation assay. Cell apoptosis and metastasis were detected by flow cytometry analysis and transwell assay, respectively. The binding relationship between circSCAF11 and miR-145-5p was predicted by circular RNA Interactome and identified by dual-luciferase reporter assay and RNA immunoprecipitation assay. In vivo tumor formation assay was performed to reveal the effects between ropivacaine and circSCAF11 overexpression on tumorigenesis in vivo. Results CircSCAF11 expression was obviously upregulated and miR-145-5p was significantly downregulated in glioma tissues and cells compared with control groups. Ropivacaine treatment upregulated E-cadherin protein expression and repressed the protein expression of Vimentin. Functionally, ropivacaine exposure promoted ROS and 8-OHdG production and cell apoptosis, whereas inhibited cell proliferation, migration and invasion; however, these effects were hindered by circSCAF11 overexpression. Mechanistically, circSCAF11 was a sponge of miR-145-5p. In addition, ropivacaine was revealed to inhibit tumor growth in vivo by regulating circSCAF11 and miR-145-5p expression. Conclusion Ropivacaine suppressed glioma progression by regulating circSCAF11 and miR-145-5p, which might provide a theoretical foundation in glioma treatment.

Ropivacaine suppresses tumor biological characteristics of human hepatocellular carcinoma via inhibiting IGF-1R/PI3K/AKT/mTOR signaling axis

“…Furthermore, ropivacaine significantly promotes apoptosis in multiple cancers [ 33 , 44 , 53 ]. PARP and caspase 3 are considered crucial components of the apoptotic cascade [ 54 , 55 ].…”

“…Accumulating evidence suggests that ropivacaine inhibits the migration and invasion of diverse cancers, such as esophageal and papillary thyroid cancers [ 16 , 36 ] and ultimately achieves the goal of anti-tumor therapy. Ropivacaine treatment upregulates E-cadherin expression and represses vimentin expression in glioma cells, resulting in metastasis inhibition [ 44 ]. The anti-metastatic effect of ropivacaine may be via impeding Src-activation and intercellular adhesion molecule-1 phosphorylation, thus hindering EMT progression [ 58 ].…”

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

“…Besides miRNAs and LncRNAs, current studies have implied circRNAs are also capable of participating in OS-mediated cancer metastasis. CircSCAF11 overexpression inhibited ROS production by acting as a sponge of miR-145-5p in glioma, which is a cause of glioma initiation and metastasis [ 85 ]. MiR-30c-5p was reported to be an important OS regulator by multiple studies [ 86 – 88 ].…”

Ropivacaine Inhibits Wound Healing by Suppressing the Proliferation and Migration of Keratinocytes via the PI3K/Akt/mTOR Pathway

“…Accumulating studies have proved that ropivacaine exhibits anti-proliferative and anti-migratory activities on numerous cells [23][24][25][26]. For example, ropivacaine inhibits proliferation and promotes apoptosis of SH-SY5Y cells (human neuroblastoma cell line) in a dose-and time-dependent manner to induce neuronal injury [27].…”