LncRNA HULC promoted bladder cancer cells proliferation and inhibited apoptosis.

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 smallinterfering-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.

MicroRNA (miR)-21 has many regulatory functions in the cell, including activities in cancer cells and cancer stem cells. Large tumor suppressor gene 1 (LATS1) is a target of miR-21 that could mediate several of these phenotypes. This study explored the effect of miR-21 silencing in renal cancer cell function and LATS1 expression. Silencing of miR-21 in Caki-2 cells reached an efficiency of 55–60%. This was sufficient to detect decrease in Caki-2 cell proliferation and migration invasion capacity. miR-21 silencing increased LATS1 expression at both mRNA and protein levels. The number of tumor spheres formed by cells expressing si-miR-21 was significantly reduced and the expression of tumor stem cell markers Nanog and CT3/4 were significantly downregulated. miR-21 seems to regulate LATS1 expression in renal cancer Caki-2 cells, resulting in reduced proliferation, invasion, and cancer stem cell phenotype. miR-21 may promote malignant phenotype of tumor cells through LATS1 silencing, which can be regarded as a new target candidate gene for renal cancer treatment.