miR-16-5p may modulate migration and proliferation through TP53 and LncRNA-NEAT1 in triple-negative breast cancer

IF 1 Q4 GENETICS & HEREDITY

Gene Reports Pub Date : 2024-09-20 DOI:10.1016/j.genrep.2024.102038

引用次数: 0

Abstract

Introduction

MicroRNAs (miRNAs) are potential candidate clinical biomarkers for many diseases. This study explored the role and potential mechanisms of miR-16-5p in triple-negative breast cancer (TNBC).

Results

The expression of miR-16-5p was lower in wax block sections obtained from 47 TNBC patient samples. Overexpression of miR-16-5p decreased the migratory abilities and the cell proliferation in MDA-MB-231 cells. We found miR-16-5p modulated TP53 and LncRNA-NEAT1 in bioinformatics analysis. In transfection experiments, the higher expression of lncRNA-NEAT1 and TP53 were observed in miR-16-5p inhibitor group.

Conclusion

Our data demonstrated that miR-16-5p was lowly expressed and acted as a tumor suppressor in TNBC. Moreover, miR-16-5p regulated TNBC cell proliferation and migratory capacity by modulating TP53 and lncRNA-NEAT1 in vitro.

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miR-16-5p 可通过 TP53 和 LncRNA-NEAT1 调节三阴性乳腺癌的迁移和增殖

导言微小RNA（miRNA）是许多疾病潜在的候选临床生物标记物。本研究探讨了 miR-16-5p 在三阴性乳腺癌（TNBC）中的作用和潜在机制。过表达 miR-16-5p 会降低 MDA-MB-231 细胞的迁移能力和细胞增殖。我们在生物信息学分析中发现，miR-16-5p 可调节 TP53 和 LncRNA-NEAT1。结论我们的数据表明，miR-16-5p 在 TNBC 中低表达，并作为肿瘤抑制因子发挥作用。此外，miR-16-5p 在体外通过调节 TP53 和 lncRNA-NEAT1 来调控 TNBC 细胞的增殖和迁移能力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.