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Exploring the regulatory role of FBXL19-AS1 in triple-negative breast cancer through the miR-378a-3p/OTUB2 axis
Chenxu Guo1,2,3, Mingliang Zhang3, Xin Jin3
1Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Cell Biochemistry and Function
|May 4, 2024
Summary
Long noncoding RNA FBXL19-AS1 promotes triple-negative breast cancer (TNBC) by suppressing miR-378a-3p, increasing OTUB2 expression. This mechanism involves the Hippo signaling pathway, offering potential therapeutic targets for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNA (lncRNA) FBXL19-AS1's role in triple-negative breast cancer (TNBC) is not well-defined.
- Understanding lncRNA regulation is crucial for developing novel cancer therapies.
Purpose of the Study:
- To investigate the function and mechanism of FBXL19-AS1 in TNBC.
- To identify potential therapeutic targets for TNBC treatment.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for gene expression analysis.
- Cellular assays (flow cytometry, CCK-8, Transwell) to assess cell activity.
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays for molecular interactions.
- In vivo xenograft models for tumor growth evaluation.
Main Results:
- FBXL19-AS1 was upregulated in TNBC tissues and cell lines.
- FBXL19-AS1 knockdown inhibited TNBC cell proliferation and tumorigenesis.
- FBXL19-AS1 sponged miR-378a-3p, which targets and downregulates OTUB2.
- The miR-378a-3p/OTUB2 axis influences the Hippo signaling pathway.
Conclusions:
- FBXL19-AS1 promotes TNBC progression by inhibiting miR-378a-3p and upregulating OTUB2.
- The FBXL19-AS1/miR-378a-3p/OTUB2 axis, potentially involving the Hippo pathway, represents a novel therapeutic strategy for TNBC.
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