In:
Journal of Cellular Biochemistry, Wiley, Vol. 121, No. 3 ( 2020-03), p. 2236-2246
Abstract:
We explored the roles and regulatory mechanisms of the circular RNA (circRNA) nuclear receptor‐interacting protein 1 (NRIP1; circNRIP1) in ACHN and CAKI‐1 cells. ACHN and CAKI‐1 cells were transfected with small‐interfering‐circNRIP1 (si‐circNRIP1) and microRNA‐505 (miR‐505) inhibitor or the corresponding controls. Cell viability was detected with the Cell Counting Kit‐8. The protein expression levels of Bcl‐2, Bax, cleaved‐caspase‐3, matrix metalloproteinase (MMP)‐2, MMP‐9, adenosine 5′‐monophosphate (AMP)‐activated protein kinase (AMPK), protein kinase B (AKT), phosphatidylinositol 3‐kinase (PI3K), and mammalian target of rapamycin (mTOR) were individually determined via Western blot. Quantitative reverse transcription polymerase chain reaction was used to examine the expressions of circNRIP1 and miR‐505 both in tumor cells and tissues. The apoptotic rate, the colony numbers, and the migration rate were separately determined by the Annexin V‐fluorescein isothiocyanate/propidium iodide and flow cytometer, colony formation assay, and migration assay. We found that circNRIP1 was overexpressed in tumor tissue but miR‐505 was overproduced. Silencing circZNF292 induced inhibition of cell viability, colony formation, and migration, as well as the activity of AMPK and PI3K/AKT/mTOR cascades but enhancement of apoptosis. si‐circNRIP1 stimulated the upregulation of miR‐505, whose silence abolished the effects of si‐circNRIP1 on these elements mentioned above. In conclusion, the circNRIP1 played oncogenic roles in the ACHN and the CAKI‐1 cell lines by targeting miR‐505 via stimulating AMPK and PI3K/AKT/mTOR cascades.
Type of Medium:
Online Resource
ISSN:
0730-2312
,
1097-4644
Language:
English
Publisher:
Wiley
Publication Date:
2020
detail.hit.zdb_id:
1479976-5
SSG:
12
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