MicroRNA-424 serves an anti-oncogenic role by targeting cyclin-dependent kinase 1 in breast cancer cells

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Abstract

The aim of the present study was to define the function of microRNA-424-5p (miR-424) in breast cancer cells. The present study investigated the level and the potential function of miR-424 in breast cancer by reverse transcription-quantitative polymerase chain reaction assays. miR-424 expression was decreased in the majority of human breast cancer specimens and cell lines used in the present study. The MTT assay, plate colony formation assay and flow cytometry analyses were used to characterize the function of miR-424 in two types of breast cancer cell lines. Upregulation of miR-424 inhibited cellular proliferation and regulated the cell cycle by arresting cells in the G2/M cell phase. The dual-luciferase reporter assay was used to confirm the direct association between miR-424 and cyclin-dependent kinase 1 (CDK1). Silencing of CDK1 expression by CDK1 short interfering RNA also significantly suppressed cell proliferation and arrested cells in the G2/M cell phase. The results of the present study indicated that miR-424 can suppress cell proliferation and arrest cells in G2/M cell phase by negatively regulating CDK1 mRNA in human breast cancer, possibly through the Hippo pathway and the extracellular signal-regulated kinase pathway. The results of the present study provided novel evidence for the role of miR-424 in breast cancer.

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Cdk1 is sufficient to drive the mammalian cell cycle.

David Santamaría, Cédric Barrière, Antonio Cerqueira … (2007)

Unicellular organisms such as yeasts require a single cyclin-dependent kinase, Cdk1, to drive cell division. In contrast, mammalian cells are thought to require the sequential activation of at least four different cyclin-dependent kinases, Cdk2, Cdk3, Cdk4 and Cdk6, to drive cells through interphase, as well as Cdk1 to proceed through mitosis. This model has been challenged by recent genetic evidence that mice survive in the absence of individual interphase Cdks. Moreover, most mouse cell types proliferate in the absence of two or even three interphase Cdks. Similar results have been obtained on ablation of some of the activating subunits of Cdks, such as the D-type and E-type cyclins. Here we show that mouse embryos lacking all interphase Cdks (Cdk2, Cdk3, Cdk4 and Cdk6) undergo organogenesis and develop to midgestation. In these embryos, Cdk1 binds to all cyclins, resulting in the phosphorylation of the retinoblastoma protein pRb and the expression of genes that are regulated by E2F transcription factors. Mouse embryonic fibroblasts derived from these embryos proliferate in vitro, albeit with an extended cell cycle due to inefficient inactivation of Rb proteins. However, they become immortal on continuous passage. We also report that embryos fail to develop to the morula and blastocyst stages in the absence of Cdk1. These results indicate that Cdk1 is the only essential cell cycle Cdk. Moreover, they show that in the absence of interphase Cdks, Cdk1 can execute all the events that are required to drive cell division.

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Targeting CDK4 and CDK6: From Discovery to Therapy.

Charles J Sherr, David A Beach, Geoffrey I Shapiro (2016)

Biochemical and genetic characterization of D-type cyclins, their cyclin D-dependent kinases (CDK4 and CDK6), and the polypeptide CDK4/6 inhibitor p16(INK4)over two decades ago revealed how mammalian cells regulate entry into the DNA synthetic (S) phase of the cell-division cycle in a retinoblastoma protein-dependent manner. These investigations provided proof-of-principle that CDK4/6 inhibitors, particularly when combined with coinhibition of allied mitogen-dependent signal transduction pathways, might prove valuable in cancer therapy. FDA approval of the CDK4/6 inhibitor palbociclib used with the aromatase inhibitor letrozole for breast cancer treatment highlights long-sought success. The newest findings herald clinical trials targeting other cancers.

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MicroRNAs: New Biomarkers for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Breast Cancer

Gloria Bertoli, Claudia Cava, Isabella Castiglioni (2015)

Dysregulation of microRNAs (miRNAs) is involved in the initiation and progression of several human cancers, including breast cancer (BC), as strong evidence has been found that miRNAs can act as oncogenes or tumor suppressor genes. This review presents the state of the art on the role of miRNAs in the diagnosis, prognosis, and therapy of BC. Based on the results obtained in the last decade, some miRNAs are emerging as biomarkers of BC for diagnosis (i.e., miR-9, miR-10b, and miR-17-5p), prognosis (i.e., miR-148a and miR-335), and prediction of therapeutic outcomes (i.e., miR-30c, miR-187, and miR-339-5p) and have important roles in the control of BC hallmark functions such as invasion, metastasis, proliferation, resting death, apoptosis, and genomic instability. Other miRNAs are of interest as new, easily accessible, affordable, non-invasive tools for the personalized management of patients with BC because they are circulating in body fluids (e.g., miR-155 and miR-210). In particular, circulating multiple miRNA profiles are showing better diagnostic and prognostic performance as well as better sensitivity than individual miRNAs in BC. New miRNA-based drugs are also promising therapy for BC (e.g., miR-9, miR-21, miR34a, miR145, and miR150), and other miRNAs are showing a fundamental role in modulation of the response to other non-miRNA treatments, being able to increase their efficacy (e.g., miR-21, miR34a, miR195, miR200c, and miR203 in combination with chemotherapy).

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Author and article information

Journal

Journal ID (nlm-ta): Oncol Rep

Journal ID (iso-abbrev): Oncol. Rep

Title: Oncology Reports

Publisher: D.A. Spandidos

ISSN (Print): 1021-335X

ISSN (Electronic): 1791-2431

Publication date (Print): December 2018

Publication date (Electronic): 27 September 2018

Publication date PMC-release: 27 September 2018

Volume: 40

Issue: 6

Pages: 3416-3426

Affiliations

[1 ]Department of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, Shanghai 200072, P.R. China

[2 ]Medical College of Soochow University, Suzhou, Jiangsu 215123, P.R. China

[3 ]Tongji University School of Medicine, Shanghai 200092, P.R. China

[4 ]Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China

Author notes

Correspondence to: Professor Lin Fang or Dr Dan Xie, Department of Breast and Thyroid Surgery, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, 301 Yanchang Road, Shanghai 200072, P.R. China, E-mail: fanglin2017@ 123456126.com , E-mail: grace_579@ 123456163.com

Article

Publisher ID: or-40-06-3416

DOI: 10.3892/or.2018.6741

PMC ID: 6196586

PubMed ID: 30272324

SO-VID: 9d1f4c90-f7e2-4f02-95c2-0cf30b1b77fe

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

History

Date received : 10 April 2018

Date accepted : 17 September 2018

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MicroRNA-424 serves an anti-oncogenic role by targeting cyclin-dependent kinase 1 in breast cancer cells

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Most cited references 25

Cdk1 is sufficient to drive the mammalian cell cycle.

Targeting CDK4 and CDK6: From Discovery to Therapy.

MicroRNAs: New Biomarkers for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Breast Cancer

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