Circular RNA circ_0001162 promotes cell proliferation and invasion of glioma via the miR-936/ERBB4 axis

As a new type of non-coding RNA, the role of circular RNA (circRNA) in various diseases and tumors has received considerable attention. Studies have shown that circRNAs play an important role in the progression of acute myeloid leukemia (AML) via different mechanisms. However, the specific underlying molecular mechanism of circRNAs in the proliferation of AML cells remians unclear. This study aimed to clarify the biological role and mechanism of circCRKL in AML. The results indicated low circCRKL expression in AML cell lines and samples. Moreover, the overexpression of circCRKL inhibited the proliferation and colony-forming ability of AML cells, while its silencing promoted them. In addition, bioinformatics tools and luciferase assays revealed that circCRKL could sponge miR-196a-5p and miR-196b-5p to promote the expression of p27. Furthermore, circCRKL inhibited AML cell proliferation via the miR-196a-5p/miR-196b-5p/p27 axis, suggesting a potential new target for AML therapy.

Section: Discussionmentioning

confidence: 99%

“…The clones were stained with MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (Sigma, USA, Cat no. M5655) and scored after 10–14 days [ 19 ].…”

Section: Methodsmentioning

confidence: 99%

Circular RNA circCRKL inhibits the proliferation of acute myeloid leukemia cells via the miR-196a-5p/miR-196b-5p/p27 axis

Liu

Cheng

2021

“…It is reported that miR-182 inhibits the invasive phenotype of esophageal squamous cell cancer cells by regulating MYC proto-oncogene[ 33 ]. Another study reports that miR-936 inhibits glioma progression by regulating ErbB2 receptor tyrosine kinase 4[ 34 ]. MiR-582-5p is reported to be aberrantly expressed in diverse human cancers, including osteosarcoma, bladder cancer, non-small cell lung cancer (NSCLC), and endometrial cancer [ 35–38 ].…”

Section: Discussionmentioning

confidence: 99%

TTK (threonine tyrosine kinase) regulates the malignant behaviors of cancer cells and is regulated by microRNA-582-5p in ovarian cancer

Lü

Ren

2021

There is growing evidence that threonine tyrosine kinase (TTK) dysregulation is linked to the progression of multiple malignancies. Nonetheless, the role of TTK in ovarian cancer (OC) remains unclear. The GEO2R method was employed to screen out the mRNAs that were abnormally expressed between OC tissues and normal ovarian tissues using three datasets from the Gene Expression Omnibus (GEO) database: GSE14407, GSE18520, and GSE36668. Moreover, the Kaplan-Meier plotter was utilized to investigate the association between TTK expression and OC patients' prognosis. Furthermore, quantitative real-time PCR (qRT-PCR) was applied to examine miR-582-5p expression and TTK mRNA expression in OC tissues and cells. Additionally, immunohistochemistry (IHC) experiment and Western blot were executed to examine TTK protein expression in OC tissues and cells, respectively. In addition, Cell Counting Kit-8 (CCK-8), transwell, and flowcytometry experiments were performed to examine the multiplication, migration, and apoptosis of OC cells, respectively. In addition, dual-luciferase reporter gene tests were executed to validate the targeting relationship between miR-582-5p and TTK. We demonstrated that TTK expression was up-regulated in OC tissues and cells, and its overexpression was found to be associated with an adverse prognosis in OC patients. TTK overexpression enhanced OC cell multiplication and migration, and repressed apoptosis. Mechanistically, TTK was a downstream target of miR-582-5p. Furthermore, miR-582-5p overexpression impeded OC cell multiplication and migration, while TTK overexpression reversed this phenomenon. These data suggest that miR-582-5p and TTK are promising targets for OC diagnosis and therapy.

“…RNA pull-down assay was performed using an RNA pull-down kit (Bes5102, Bersin Biotechnology Co., Ltd.) according to a previous study [ 26 ]. Abiocenter (Beijing) Biotechnology Co., Ltd synthesized the biotinylated miR-380-5p probe and its control probe.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA AC012668 suppresses non-alcoholic fatty liver disease by competing for microRNA miR-380-5p with lipoprotein-related protein LRP2

Chen

Gao

et al. 2021

Nonalcoholic fatty liver disease (NAFLD) is characterized by high morbidity. Although long noncoding RNAs (lncRNAs) are known to have a role in NAFLD pathogenesis, the identified lncRNA types are limited. In this study, NAFLD models were established in vitro and in vivo using free fatty acid-treated LO2 cells and high-fat diet-fed mice, respectively. Microarray data were downloaded from the Gene Expression Omnibus database, and AC012668 was selected for further analysis. Cell viability and apoptosis were measured using Cell Counting Kit 8 and flow cytometry assays. RNA expression was detected using reverse transcription-quantitative polymerase chain reaction. Triglyceride (TG) content and lipid deposition were detected using enzymelinked immunosorbent assay and Oil-Red O staining. Western blotting was used to visualize protein expression. Starbase and TargetScan were used to predict the target miRNA and gene, and the predictions were verified through RNA pull-down and luciferase reporter assays. AC012668 expression levels were significantly suppressed in NAFLD models, whereas AC012668 overexpression inhibited lipogenesis-related gene (SCD1, SREBP1, FAS) expression and TG/lipid accumulation in vitro. Subsequently, miR-380-5p was predicted and verified to target AC012668, and its expression was notably increased in the NAFLD cell model. Moreover, transfection of miR-380-5p antagonized the effects of AC012668 on lipid formation and accumulation. LRP2 was confirmed to be the target gene of miR-380-5p and was downregulated in the NAFLD cell model. Silencing LRP2 reversed the effects of the miR-380-5p inhibitor on lipid formation and accumulation. AC012668 inhibited NAFLD progression via the miR-380-5p/LRP2 axis. These findings may provide a novel strategy against NAFLD.