These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Silence of cZNF292 suppresses the growth, migration, and invasion of human esophageal cancer Eca-109 cells via upregulating miR-206.
    Author: Liu Z, Hu G, Zhao Y, Xiao Z, Yan M, Ren M.
    Journal: J Cell Biochem; 2020 Mar; 121(3):2354-2362. PubMed ID: 31680303.
    Abstract:
    Circular RNA (circRNA) cZNF292 has been previously revealed as a circular oncogenic RNA. This study attempted to illustrate the functions of cZNF292 in human esophageal carcinoma Eca-109 cells. Eca-109 cells were transfected with the short hairpin RNA specific against cZNF292 (sh-cZNF292) and/or miR-206 inhibitor. cZNF292 and miR-206 expression was examined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Cell counting kit-8 and flow cytometry were performed for detecting cell growth including cell viability as well as apoptosis. Various kinds of factors, which are involved in cell development including proliferation, apoptosis, migration, and invasion were determined by western blot analysis. Besides, the activation of AMP-activated protein kinase (AMPK) and PI3K/AKT signaling was measured by western blot analysis. It was found that cZNF292 silencing decreased Eca-109 cell viability and induced apoptosis. In the meantime, cZNF292 silencing inhibited cell migration and invasion. cZNF292 silencing upregulated miR-206 expression. And miR-206 downregulation impaired the suppressive effects of cZNF292 silence toward Eca-109 cell growth, migration, and invasion. cZNF292 silencing activated AMPK signaling and inactivated PI3K/AKT signaling also via regulating miR-206. In conclusion, silencing of cZNF292 abated growth, migration, and invasion of Eca-109 cells by upregulating miR-206, which subsequently modulated AMPK and PI3K/AKT signaling pathways.
    [Abstract] [Full Text] [Related] [New Search]