Cisatracurium inhibits the growth and induces apoptosis of ovarian cancer cells by promoting lincRNA-p21

Abstract

As a common muscle relaxant, cisatracurium has shown good antitumor effect on some tumors. Recent studies reported that cisatracurium could inhibit the progression of colon cancer by upregulating tumor suppressor gene p53. However, its role in ovarian cancer and its regulatory effect on p53 and p53 downstream targeting gene long intergenic noncoding RNA p21 (lincRNA-p21) is still unknown. Quantitative Real-time Polymerase Chain Reaction (qRT-PCR) was used to assess the expression of p53, lincRNA-p21 and miR-181b. Cell viability and proliferation were detected by CCK-8 assay and Edu staining, respectively. Wound-healing and Transwell assays were performed to determine the abilities of cell migration and invasion. Apoptosis was evaluated by TUNEL staining. Luciferase reporter assay was conducted to detect the relationship between lincRNA-p21 and miR-181b. As a result, cisatracurium could increase the expressions of p53 and lincRNA-p21 of ovarian cancer cell line (OVCAR-3) in a dose-dependent manner. In addition, cisatracurium significantly inhibited the proliferation, migration and invasion of OVACR-3 cells, and induced apoptosis. However, these above changes in biological function can be attenuated by lincRNA-p21 knockdown. Next, lincRNA-p21 could directly target miR-181b and negatively regulate its expression by luciferase reporter assay. In conclusion, cisatracurium inhibited the progression of OVCAR-3 cells through upregulation of lincRNA-p21 expression activated by p53 inhibiting miR-181b expression. The experimental results provide a new research idea for the application of cisatracurium in ovarian cancer.

Fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6)

“…Then, we further probed whether fluvastatin exerted protective effects on EC progression via knocking down SIRT6 expression. However, the role of PI3K-mTOR pathway in the mechanism of action of fluvastatin related to SIRT6 still requires further study [ 23 , 24 ]. It was obviously found that depletion of SIRT6 triggered more activated cell viability and stimulated the behaviors of EC cells, including proliferation, migration, invasion.…”

Identification and validation of a five-lncRNA signature for predicting survival with targeted drug candidates in ovarian cancer

“…Molecular targets and pathways currently under investigation for drug development in ovarian cancers include, cell cycle inhibitors, mTOR inhibitors, and PI3K inhibitors. A recent study found that cisatracurium can inhibit the progression of OC cells by upregulating lncRNA-p21 activated by p53 inhibiting miR-181b expression, indicating that drugs targeting ceRNA networks are indeed promising in treating OC [ 34 ]. In our study, we found five small-molecule drugs with potential therapeutic efficacy based on OC RNA-seq using bioinformatics analysis, thus guiding the direction for future drug exploration.…”

Omarigliptin ameliorated high glucose-induced nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation through activating adenosine monophosphate-activated protein kinase α (AMPKα) in renal glomerular endothelial cells

“…Cell viability of treated HrGECs was determined with a CCK-8 assay. To determine the cell viability, HrGECs were mixed with 10 µL CCK-8 solution and incubated at 37°C for 2 hours, followed by measuring the absorbance at 450 nm using a microplate reader (J&H technology Co., Ltd, Jiangsu, China) [ 15 ].…”