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Updated: Oct 31, 2025

Monitoring of Nanodrug Accumulation in Murine Breast Cancer Metastases
Published on: August 23, 2024
Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1
Weipeng Liu1, Xin Zhou1, Yuanqiang Li1
1Department of General Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang Central People's Hospital, Yichang, China.
Purpose:
Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified.
Methods:
Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays. Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p. Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting.
Results:
NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD.
Conclusion:
NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.
Insights
Non-coding RNA activated by DNA damage (NORAD) suppresses breast cancer progression by inhibiting microRNA-155-5p, leading to increased suppressor of cytokine signaling 1. This finding offers new insights into breast cancer (BC) treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) play crucial roles in cancer development.
- Non-coding RNA activated by DNA damage (NORAD) is implicated in various cancers, but its function in breast cancer (BC) remains unclear.
Purpose of the Study:
- To investigate the role of NORAD in breast cancer (BC).
- To elucidate the molecular mechanism of NORAD in regulating BC cell malignancy.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
- Western blotting for protein expression.
- Cell proliferation, migration, and invasion assays (CCK-8, BrdU, Transwell).
- Bioinformatics, RNA immunoprecipitation (RIP), and dual-luciferase reporter assays to confirm molecular interactions.
Main Results:
- NORAD expression was significantly downregulated in BC tissues and cell lines, correlating with poor differentiation.
- NORAD overexpression inhibited BC cell proliferation, migration, and invasion, while knockdown promoted these processes.
- NORAD directly targeted microRNA (miR)-155-5p, and miR-155-5p targeted suppressor of cytokine signaling 1 (SOCS1).
- NORAD suppressed miR-155-5p, leading to SOCS1 upregulation.
Conclusions:
- NORAD acts as a tumor suppressor in breast cancer (BC).
- The NORAD/miR-155-5p/SOCS1 axis regulates BC cell proliferation, migration, and invasion.
- NORAD suppresses miR-155-5p to upregulate SOCS1, thereby inhibiting BC progression.
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