Home > Riviste > Minerva Medica > Fascicoli precedenti > Articles online first > Minerva Medica 2020 Jul 17

ULTIMO FASCICOLO
 

JOURNAL TOOLS

eTOC
Per abbonarsi
Sottometti un articolo
Segnala alla tua biblioteca
 

ARTICLE TOOLS

Publication history
Estratti
Permessi
Per citare questo articolo

 

 

Minerva Medica 2020 Jul 17

DOI: 10.23736/S0026-4806.20.06639-2

Copyright © 2020 EDIZIONI MINERVA MEDICA

lingua: Inglese

Circular RNA circFANCL motivates the glioma progression via the action on the miR-337-3p/HMGB1 signal axis

Wang TAO 1, Zhou JIA 2 , Wu MENGSHI 3, Luo WEI 4, Liang FENG 5

1 Department of Neurosurgery, The Second Affiliated Hospital of South China University, Hengyang, Hunan Province, China; 2 Department of Emergency, The First Affiliated Hospital of South China University, Hengyang, Hunan province, China; 3 Department of Water Resources, Hydrology and Water Resources Survey Bureau of Hengyang, Hengyang, Hunan Province, China; 4 Department of Internal Medicine-Cardiovascular, The First Affiliated Hospital of
South China University, Hengyang, Hunan Province, China; 5 Department of Anesthesiology, The First Affiliated Hospital of South China University, Hengyang, Hunan Province, China


PDF


BACKGROUND: Circular RNAs (circRNAs) are significant modulatory molecules in the developing process of glioma. Our study will emphasize on exploring the function of circRNA Fanconi anemia group L protein (circFANCL) and the specific mechanism in glioma.
METHODS: The quantitative real-time polymerase chain reaction (qRT-PCR) was implemented for detecting circFANCL, microRNA-337-3p (miR-337-3p) and high mobility group box-1 (HMGB1). Cell proliferation analysis was assessed using Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied to determine cell cycle and apoptosis. All protein detection was completed by western blot. Animal experiment was performed to investigate the role of circFANCL in vivo. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were collectively conducted for analyzing the targeted combination.
RESULTS: CircFANCL was signally increased in glioma tissues and cells, and the up-regulated circFANCL could predict poor prognosis in clinical glioma patients. Down-regulated circFANCL induced the proliferation inhibition, cell cycle arrest and apoptosis promotion of glioma cells in vitro, and inhibited tumor growth in vivo. Regarding the mechanism, circFANCL served as a sponge of miR-337-3p that was a tumor suppressor in glioma and circFANCL targeted miR-337-3p to regulate HMGB1 that was a target gene of miR-337-3p. Furthermore, HMGB1 down-regulation was responsible for the repression of glioma progression caused by knockdown of circFANCL.
CONCLUSIONS: Through the illustration of oncogenic function of circFANCL in glioma by the miR-337-3p/HMGB1 axis, we believed that circFANCL might be a great target in the early diagnosis and late treatment of glioma.


KEY WORDS: CircFANCL; Glioma; miR-337-3p; HMGB1

inizio pagina