Notes

circ-ACACA stimulates spreading, intrusion, migration and glycolysis associated with cervical most cancers cellular material through individuals miR-582-5p/ERO1A signaling axis.
In a word, this work illustrated the regulatory function of KIF22/miR-122 axis in ESSC and provided potential targets for potential targets for ESSC treatment.Atherosclerosis, a chronic inflammatory disease, is the primary cause of most cardiovascular diseases. Tyloxapol mouse Circular RNAs (circRNAs) were reported to serve as post-transcriptional regulators and diagnostic markers in various diseases, but the underlying correlation between circRNAs and atherosclerosis remains elusive. In this study, we downloaded the microarray dataset GSE107522 from the Gene Expression Omnibus (GEO) and identified nine differentially expressed circRNAs (DECs). DECs expression in exosomes were investigated, and hsa_circ_0005699 was selected for subsequent analysis. We then identified 14 RNA-binding proteins (RBPs) and 71 possible hsa_circ_0005699-interacting microRNAs. Subsequently, target gene prediction and enrichment analyses were performed. The enriched pathways of RBP eIF4AIII include spliceosome, cell cycle, and pathways in cancer. We constructed a protein-protein interaction network, and 20 hub genes were identified using Search Tool for the Retrieval of Interacting Genes/Proteins and Cytoscape. Hub gene analysis revealed significant enrichment in mRNA splicing via the spliceosome, RNA splicing, protein binding, neurotrophin signaling pathway, and Ras signaling pathway. Using DrugMatrix of the Enrichr database, we identified 16 most significant small-molecule compounds that interacted with hub genes. Finally, seven hub genes (NEDD4L, FBXO44, FBXO27, WSB1, FBXW8, UBE2F, and ASB1) in cluster 1 were considered key targets associated with atherosclerosis according to MCODE analysis and the intersection between the module and hub genes. Thus, hsa_circ_0005699, RBP eIF4AIII, and the seven identified hub genes (NEDD4L, FBXO44, FBXO27, WSB1, FBXW8, UBE2F, and ASB1) could help to elucidate the pathogenesis and progression of atherosclerosis. This work may contribute to providing candidate targets for the diagnosis and treatment of atherosclerosis.
We aimed to investigate the mechanism of circular RNA circ_0084927 in the progression of breast cancer (BC).

The levels of circ_0084927, miR-142-3p, and ELKS/RAB6-interacting/CAST family member-1 (ERC1) mRNA in the BC tissues and cells were detected by qRT-PCR. CCK8, colony formation, Transwell, and flow cytometry assays were performed to examine the cell proliferation, colony formation, cell invasion, and apoptosis, respectively, in the BC cells with regulated expressions of circ_0084927, miR-142-3p, and ERC1. RNase R treatment was employed to verify the circular structure of circ_0084927. Nucleocytoplasmic separation experiment, bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation were performed to investigate the ceRNA mechanism of circ_0084927.

High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05).

Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis.
Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis.
To investigate the effects of 5-aza-2'-deoxycytidine (5-AZA-DC) on preeclampsia (PE) and functional mechanisms dependent on STAT3.

Trophoblastic cells (HTR8/Svneo, JEG-3, JAR and BeWo) were used to constructed STAT3-overexpressing or -silenced cells. qRT-PCR, Western blot, and FISH were used to detect mRNA and protein expression. GST-pull down, ChIP and dual luciferase reporter were used to prove the association of STAT3 and PTEN or TSC2, LC-MS/MS for proteome, and MeDIP-Seq for transcriptome. CCK-8 and flow cytometry were used to examine cell proliferation and apoptosis. C57BL/6J mice were divided into 4 groups (control, control + 5-AZA-DC, PE and PE + 5-AZA-DC). Systolic blood pressure, 24-h urinary protein, APTT, D-D, PT, ALT, Scr, and BUN were determined. Placental blood flow velocity was detected by Doppler ultrasound, HE staining for kidney injury.

STAT3, PTEN and TSC2 were the dominantly differential expressed genes in preeclampsia. Aberrant STAT3 expression increased DNMT1 levels. STAT3 regulated PTEN promoter activity. STAT3 interacted with PTEN and TSC2. DNMT1 was increased while STAT3, PTEN and TSC2 were decreased by 5-AZA-DC. Cell proliferation was promoted and apoptosis was inhibited by 5-AZA-DC. PE-induced STAT3 down-regulation was restored by 5-AZA-DC. Systolic blood pressure, 24-h urinary protein, APTT, D-D, PT, ALT, Scr and BUN were increased, and velocity of placental blood flow was inhibited in PE compared with control mice, while 5-AZA-DC relived these indicators.

Preeclampsia symptoms was relieved by 5-AZA-DC, suggesting that 5-AZA-DC could be used as a potential drug for epigenetic treatment of preeclampsia.
Preeclampsia symptoms was relieved by 5-AZA-DC, suggesting that 5-AZA-DC could be used as a potential drug for epigenetic treatment of preeclampsia.Classical aluminum adjuvant is a deficient antigen carrier for cross-presentation and cross-priming of CD8+ cytotoxic T cells. Our previous research has demonstrated that cross-presentation efficiency significantly increased when antigens are conjugated covalently to α-Al2O3 nanoparticles. Here we found that coating conventional aluminum adjuvants with polyethyleneimine (PEI) could enhance antigen cross-presentation of DCs (dendritic cells) in vitro and in vivo. PEIs exerted differential effects on antigen cross-presentation. These findings provided an alternative approach to promote the rapid translation of alumina nanoparticles adjuvants into clinical application.
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