miR‑23a suppresses pancreatic cancer cell progression by inhibiting PLK‑1 expression
Corrigendum in: /10.3892/mmr.2022.12738
- Authors:
- Published online on: April 27, 2018 https://doi.org/10.3892/mmr.2018.8941
- Pages: 105-112
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Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The present study aimed to explore the effects and underlying mechanisms of microRNA (miR)‑23a on pancreatic cancer (PC) cells progression. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were used to detect the mRNA and protein miR‑23a and PLK‑1 level. Cell viability, cell cycle, migration and invasion assasy, and in vivo tumorigenicity assay were used to investigate the effects of miR‑204. Further luciferase reporter assay was used to explore the mechanisms contributing to miR‑204 effects. It was observed that miR‑23a expression was upregulated and negatively associated with polo‑like kinase‑1 (PLK‑1) expression in human PC tissues. PLK‑1 was a direct target of miR‑23a in PC cells. Functional analysis demonstrated that miR‑23a overexpression suppressed cell proliferation, inhibited cell migration and invasion and promoted cell apoptosis in vitro. When PC cells were transfected with has‑miR‑23a PLK‑1 was downregulated and its downstream molecules were deregulated, including decreased expression of B‑cell lymphoma‑2, cyclin B1 and vimentin, and increased expression of Bax and E‑cadherin. The inhibitory effect of miR‑23a on PC cell progression was observed in vivo tumor xenografts. The results of the study suggest that miR‑23a inhibits PC cell progression by directly targeting PLK‑1‑associated signaling and promoting miR‑23a expression may be a potential method for treating patients with PC.
