Knockdown of SNHG16 suppresses the proliferation and induces the apoptosis of leukemia cells via miR‑193a‑5p/CDK8
Affiliations: Clinical Laboratory, Yanbian University Hospital (Yanbian Hospital), Yanji, Jilin 133000, P.R. China, Department of Neonatology, Weinan Maternal and Child Health Hospital, Weinan, Shaanxi 714000, P.R. China
- Published online on: July 8, 2020 https://doi.org/10.3892/ijmm.2020.4671
Copyright: © Piao
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Although small nucleolar RNA host gene 16 (SNHG16) is known to exhibit auxo‑action in certain types of tumor, its role in leukemia remains unclear. The present study analyzed the role and mechanisms of action of SNHG16 in leukemia cells in order to identify therapeutic targets for this disease. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to determine SNHG16 expression in human leukemia cell lines. Using TargetScan 7.2 and dual‑luciferase reporter assay, the target genes of SNHG16 were verified. Following the downregulation of the expression of SNHG16 or its target genes, Cell Counting kit‑8 (CCK‑8) assay was performed to examine the viability of the leukemia cells. In addition, flow cytometry was performed to analyze the cell apoptotic rates, and colony formation assays were used to determine the cell proliferative ability. RT‑qPCR and western blot analysis were used to determine the association between SNHG16 and its target genes. SNHG16 was found to be abnormally highly expressed in acute myeloblastic leukemia cell lines, the knockdown of which weakened the viability of the leukemia cells, suppressed cell proliferation and promoted cell apoptosis. miR‑193a‑5p could bind to SNHG16, and its target gene was CDK8. Moreover, the expression of miR‑193a‑5p increased with the decrease in SNHG16 expression, while the inhibition of miR‑193a‑5p promoted the expression of CDK8. The downregulation of miR‑193a‑5p enhanced the viability of the leukemia cells, accelerated cell cloning and reduced cell apoptosis, which was completely opposite to the effects observed with the silencing of CDK8. The knockdown of SNHG16 suppressed the viability of the leukemia cells, suppressed cell proliferation, and induced cell apoptosis by regulating miR‑193a‑5p/CDK8. Thus, SNHG16 may prove to be a potential therapeutic target for the treatment of leukemia.