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RETRACTED ARTICLE: Circ_0069718 promotes the progression of breast cancer by up-regulating NFIB through sequestering miR-590-5p

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This article was retracted on 12 June 2023

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Abstract

Researches indicate that circular RNAs are dysregulated in breast cancer (BC) and play a critical role in regulating the malignant phenotype of cancer cells. Herein, the goal of this work was to investigate the role and mechanism of circ_0069718 in BC development. Levels of genes and proteins were detected by quantitative real-time polymerase chain reaction and western blot. In vitro experiments were performed using cell counting kit-8 assay, colony formation assay, EdU (5-ethynyl-2ʹ-deoxyuridine) assay, flow cytometry, western blot, and transwell assay, respectively. The dual-luciferase reporter and RNA immunoprecipitation assays were used to identify the target relationship between miR-590-5p and circ_0069718 or nuclear factor I/B (NFIB). In vivo experiments were conducted using Xenograft model in mice. Circ_0069718 was up-regulated in BC tissues and cells. Knockdown of circ_0069718 suppressed BC cell apoptosis, migration, and invasion in vitro effectively. Mechanistically, circ_0069718 directly targeted miR-590-5p to up-regulate its target NFIB. Rescue experiments showed that miR-590-5p inhibition reversed the inhibitory effects of circ_0069718 knockdown on BC cell-aggressive oncogenic phenotypes; moreover, miR-590-5p re-expression restrained BC cell proliferation and mobility, which were abolished by NFIB up-regulation. Besides that, circ_0069718 silencing hindered tumor growth via miR-590-5p/NFIB axis in vivo. Circ_0069718 promotes BC progression by up-regulating NFIB through sequestering miR-590-5p, suggesting a potential therapeutic strategy in BC.

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Data availability

The analyzed datasets generated during the study are available from the corresponding author on reasonable request.

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Acknowledgements

Thanks for all participants involved in this study.

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Authors and Affiliations

  1. Department of Oncology, The First People’s Hospital of Yinchuan, No. 2 Liqun West Street Xingqing District, Yinchuan, 750001, China

    Yongsheng Zhao, Xiaocha Ma & Weihua Shi

Authors
  1. Yongsheng Zhao
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  2. Xiaocha Ma
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  3. Weihua Shi
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Contributions

WS designed and supervised the study. YZ conducted the experiments and drafted the manuscript. XM collected and analyzed the data and edited the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Weihua Shi.

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Conflict of interest

The authors report no conflict of interest in this work.

Consent to participate

This study was allowed by the Animal Care and Use Committee of the First People’s Hospital of Yinchuan and performed in accordance with the guidelines of the National Animal Care and Ethics Institution.

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Not applicable.

Ethical approval

This work was permitted by the Ethics Committee of The First People’s Hospital of Yinchuan and was carried out according to the guidelines of Declaration of Helsinki, and all participants signed written informed consent.

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This article has been retracted. Please see the retraction notice for more detail: https://doi.org/10.1007/s00335-023-10001-8"

Supplementary Information

Below is the link to the electronic supplementary material.

335_2021_9923_MOESM1_ESM.tif

Fig. S1 The effects of miR-590-5p on the expression of five selected genes in breast cancer. (A, B) Western blot analysis of the levels of CBX4, KLF5, NFIB, RTN4, and SOX5 in MCF-7 and MDA-MB-231 cells transfected with miR-590-5p or miR-NC. **P < 0.01, ***P < 0.001. Supplementary file1 (TIF 319 kb)

335_2021_9923_MOESM2_ESM.tif

Fig. S2 The original pictures of migration assay and invasion assay. (A) was related to Fig. 4M, N; (B) was related to Fig. 4O, P; (C) was related to Fig. 7M, N; (D) was related to Fig. 7O, P. Supplementary file2 (TIF 12126 kb)

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Zhao, Y., Ma, X. & Shi, W. RETRACTED ARTICLE: Circ_0069718 promotes the progression of breast cancer by up-regulating NFIB through sequestering miR-590-5p. Mamm Genome 32, 517–529 (2021). https://doi.org/10.1007/s00335-021-09923-y

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  • DOI: https://doi.org/10.1007/s00335-021-09923-y

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