Lnc00113 promotes triple-negative breast cancer progression via the NOB-1/MAPK signaling axis

IF 3.2 4区医学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Journal of Gene Medicine Pub Date : 2024-02-01 DOI:10.1002/jgm.3662

Xiaoyu Li, Yunjie Jin, Jianwei Huang, Chu Feng, Xi Chen, Liang Zuo, Guyue Liu, Fei Chen, Jiashu Fan, Lin Fang

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引用次数: 0

Abstract

Background

Triple-negative breast cancer (TNBC) represents the most aggressive form of breast cancer. While the involvement of long non-coding RNA (lncRNA) in the progression of TNBC has been demonstrated, the role of Lnc00113 in TNBC remains unexplored. We aimed to explore the function of Lnc00113 in TNBC.

Methods

Expression levels and the clinical significance of Lnc00113 were assessed in The Cancer Genome Atlas (TCGA) database. The expression levels of Lnc00113 in TNBC tissues and cell lines were examined using qRT-PCR (quantitative Real-Time Polymerase chain reaction). The proliferation, apoptosis and invasion abilities were evaluated using CCK-8 (Cell Counting Kit-8), EdU (5-Ethynyl-2'-deoxyuridine), apoptosis and transwell assays following Lnc00113 knockdown/overexpression. Dual-luciferase and fluorescence in situ hybridization assays were employed to detect the correlation between Lnc00113, miR-107 and Nin-one binding protein (NOB-1).

Results

We identified significant upregulation of Lnc00113 in TNBC tissues and cell lines, with high Lnc00113 expression correlating with advanced pathological staging and poorer prognosis in the TCGA database. Functional assessments through knockdown/overexpression experiments revealed that Lnc00113 promoted TNBC cell proliferation, apoptosis and invasion. Fluorescence in situ hybridization experiments showed cytoplasmic localization of both Lnc00113 and NOB-1. Dual-luciferase assays demonstrated direct binding between Lnc00113 and miR-107, while miR-107 directly interacted with NOB-1. Mechanistically, our findings indicated that Lnc00113 promotes TNBC progression through the miR-107/NOB-1/MAPK signaling axis.

Conclusion

Lnc00113 emerges as a potential driver of TNBC growth and progression through modulation of the NOB-1/MAPK signaling axis, providing insights into diagnostic biomarkers and therapeutic targets for TNBC.

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Lnc00113通过NOB-1/MAPK信号轴促进三阴性乳腺癌的进展

三阴性乳腺癌（TNBC）是侵袭性最强的乳腺癌。虽然长非编码 RNA（lncRNA）参与 TNBC 的进展已得到证实，但 Lnc00113 在 TNBC 中的作用仍未得到探索。我们旨在探索Lnc00113在TNBC中的功能。

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

Journal of Gene Medicine 医学-生物工程与应用微生物

CiteScore

6.40

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： The aims and scope of The Journal of Gene Medicine include cutting-edge science of gene transfer and its applications in gene and cell therapy, genome editing with precision nucleases, epigenetic modifications of host genome by small molecules, siRNA, microRNA and other noncoding RNAs as therapeutic gene-modulating agents or targets, biomarkers for precision medicine, and gene-based prognostic/diagnostic studies. Key areas of interest are the design of novel synthetic and viral vectors, novel therapeutic nucleic acids such as mRNA, modified microRNAs and siRNAs, antagomirs, aptamers, antisense and exon-skipping agents, refined genome editing tools using nucleic acid /protein combinations, physically or biologically targeted delivery and gene modulation, ex vivo or in vivo pharmacological studies including animal models, and human clinical trials. Papers presenting research into the mechanisms underlying transfer and action of gene medicines, the application of the new technologies for stem cell modification or nucleic acid based vaccines, the identification of new genetic or epigenetic variations as biomarkers to direct precision medicine, and the preclinical/clinical development of gene/expression signatures indicative of diagnosis or predictive of prognosis are also encouraged.