MicroRNA‑365b‑3p represses the proliferation and promotes the apoptosis of non‑small cell lung cancer cells by targeting PPP5C Retraction in /10.3892/ol.2023.14010

Zhang,Xiaomiao; Wang,Jin; Pan,Yuqin; Zhao,Jun; Pan,Yingge; Yan,Yunqi; Shen,Zhenya

doi:10.3892/ol.2021.12650

MicroRNA‑365b‑3p represses the proliferation and promotes the apoptosis of non‑small cell lung cancer cells by targeting PPP5C

Retraction in: /10.3892/ol.2023.14010

Authors:
- Xiaomiao Zhang
- Jin Wang
- Yuqin Pan
- Jun Zhao
- Yingge Pan
- Yunqi Yan
- Zhenya Shen
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Affiliations: Department of Cardiovascular Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China, Department of Thoracic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, P.R. China, Nursing Department, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, P.R. China
Published online on: March 17, 2021 https://doi.org/10.3892/ol.2021.12650
Article Number: 389
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNA (miR)‑365b‑3p has been recently reported to induce cell cycle arrest and apoptosis in retinoblastoma; however, its expression pattern and biological function in non‑small cell lung cancer (NSCLC) remain unknown. The present study aimed to investigate the functional role of miR‑365b‑3p in NSCLC. The results demonstrated that miR‑365b‑3p expression level was significantly decreased in NSCLC tissues and cell lines compared with controls using reverse transcriptase quantitative PCR. Furthermore, miR‑365b‑3p expression level was overexpressed by miR‑365b‑3p mimics transfection in A549 cells, whereas it was downregulated following H1299 cell transfection with miR‑365b‑3p inhibitor. Restoration of miR‑365b‑3p inhibited cell proliferation, induced cell cycle G0/G1 arrest and stimulated apoptosis in A549 cells using CCK‑8 assay, colony formation and flow cytometry assay. However, miR‑365b‑3p inhibitor had the opposite effects in H1299 cells. Furthermore, results from bioinformatics analysis and luciferase reporter assay confirmed that serine/threonine protein phosphatase 5 (PPP5C) was a direct target of miR‑365b‑3p. In addition, online Kaplan‑Meier plotter software demonstrated that high PPP5C expression level was associated with lower overall survival and disease‑free survival in patients with NSCLC. Furthermore, PPP5C knockdown imitated the effects of miR‑365b‑3p mimics on A549 cell proliferation, cell cycle distribution and apoptosis, whereas its overexpression rescued the effects of miR‑365b‑3p mimics on A549 cell proliferation, cell cycle distribution and apoptosis. In conclusion, the findings from the present study suggested that miR‑365b‑3p may partly suppress NSCLC cell behaviors by targeting PPP5C, which may represent a promising therapeutic target for patients with NSCLC.

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