MicroRNA-1307-3p contributes to breast cancer progression through PRM2.

Publisher: Wiley Publishing Asia Pty Ltd Country of Publication: Singapore NLM ID: 101531441 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1759-7714 (Electronic) Linking ISSN: 17597706 NLM ISO Abbreviation: Thorac Cancer Subsets: MEDLINE

Publication: November 2012- : Singapore : Tianjin : Wiley Publishing Asia Pty Ltd ; Tianjin Lung Cancer Institute
Original Publication: Richmond, Vic. : Tianjin : Blackwell Pub. Asia Pty Ltd. ; Tianjin Lung Cancer Institute

MicroRNAs*/genetics ; Breast Neoplasms*/genetics ; Breast Neoplasms*/pathology ; Cell Movement*/genetics ; Cell Proliferation* ; Gene Expression Regulation, Neoplastic*; Humans ; Female ; Disease Progression ; Cell Line, Tumor

Background: Despite advances in screening and therapy, breast cancer (BC) remains the predominant cancer in women globally. Dysregulation of microRNAs (miRNAs) is pivotal in carcinogenesis across various cancers, including BC. Evidence indicates that miR-1307-3p is upregulated in BC tumors, yet its target genes are not fully elucidated. This study aimed to explore how miR-1307-3p regulates BC proliferation, migration, invasion, and angiogenesis and to identify potential target genes.
Methods: Basal miR-1307-3p levels were quantified in BC cell lines MDA-MB-231 and MCF-7, as well as MCF-10A using quantitative real-time reverse transcription-PCR (RT-qPCR). The impact of miR-1307-3p inhibition on BC cell proliferation, migration, invasion, and angiogenesis was assessed. Nine miRNA-target prediction databases identified potential miR-1307-3p targets. Target expression was validated using RT-qPCR, Western blot, and dual-luciferase reporter assays. MiR-1307-3p was overexpressed in MDA-MB-231 and MCF-7 compared to MCF-10A.
Results: Inhibiting miR-1307-3p significantly reduced BC cell proliferation, migration, invasion, and angiogenesis. Bioinformatics analysis identified 17 potential miR-1307-3p targets, with protamine 2 (PRM2) overexpression confirmed via Western blot and dual-luciferase assays.
Conclusion: MiR-1307-3p overexpression in BC promotes proliferation, migration, invasion, and angiogenesis. PRM2 emerges as a novel miR-1307-3p target in BC.
(© 2024 The Author(s). Thoracic Cancer published by John Wiley & Sons Australia, Ltd.)

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R25-GM061838 National Institute of General Medical Sciences-Research Training Initiative for Student Enhancement (NIGMS-RISE) Program; 5R16GM145558-02 National Institute of General Medical Sciences (NIGMS) Support for Research Excellence (SuRE) Program (R16) grant; A1-S-45974 Programa Presupuestario F003, CB2017-2018, CONAHCYT; R16 GM145558 United States GM NIGMS NIH HHS; Institutional seed funds from the University of Puerto Rico Comprehensive Cancer Center; R25 GM061838 United States GM NIGMS NIH HHS

Keywords: breast cancer; cancer progression; miR‐1307‐3p; microRNAs; protamine 2

0 (MicroRNAs)
0 (MIRN1307 microRNA, human)

Date Created: 20241009 Date Completed: 20241112 Latest Revision: 20250903

20260130

PMC11554549

10.1111/1759-7714.15460

39382427