Besides, miR-363-3p was sponged by long non-coding RNA small nucleolar RNA host gene 5 (SNHG5), which suppressed miR-363-3p expression. This research shows that SNHG5/miR-363-3p/AURKA axis partakes in CRC progression.
over 2 years ago
Journal
|
AURKA (Aurora kinase A) • MIR363 (MicroRNA 363) • SNHG5 (Small Nucleolar RNA Host Gene 5)
The silence of PDZD2 weakened the influences of PURPL overexpression on MG-63 cells and TAMs migration. On modulating the PURPL/miR-363/PDZD2 axis, TAMs-promoted OS development might be achieved.
Treatment with ASO-miR-363-3p decreased tumour size and weight in nude mice. In conclusion, miR-363-3p induced the EMT, which resulted in increased migration and invasion and reduced apoptosis in glioma cell lines, via the Wnt/β-catenin pathway by targeting CELF2.
3 years ago
Journal
|
CELF2 (CUGBP Elav-Like Family Member 2) • MIR363 (MicroRNA 363)
Our study found that propofol could inhibit invasion, migration, proliferation and EMT of RCC cells by promoting miR-363 expression and suppressing Snail1 expression.
over 3 years ago
Journal
|
CDH1 (Cadherin 1) • VIM (Vimentin) • MIR363 (MicroRNA 363)
|
CDH1 expression • VIM expression • miR-363 expression
SSFA2 was verified as a direct target of miR-363-3p, and SSFA2 overexpression partially counteracted the inhibitory effects of miR-363-3p on cell proliferation, migration and invasion in OSCC cell lines. Thus, miR-363-3p may serve as a tumor suppressor via targeting SSFA2 and may represent a potential therapeutic target for OSCC.
In addition, p-ERK expression was detected by Western blotting to observe the effects of lncRNA NORAD, miR-363-3p and PEAK1 on activation of the ERK signaling pathway. Taken together, lncRNA NORAD upregulated the expression of PEAK1 through sponging miR-363-3p, and then activated the ERK signaling pathway, thereby promoting the development of NSCLC.
over 3 years ago
Journal
|
MAPK1 (Mitogen-activated protein kinase 1) • MIR363 (MicroRNA 363)
In conclusion, miR-363 upregulation reduces detrusor fibrosis in rats with STZ-induced T2DM through suppression of the TGF-β1/Smad signaling pathway by targeting Col1a2. Therefore, our study provided further insights for the development of new therapeutic targets for T2DM.
4 years ago
Preclinical • Journal
|
SMAD4 (SMAD family member 4) • BAX (BCL2-associated X protein) • MIR363 (MicroRNA 363) • SMAD7 (SMAD Family Member 7)