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lncSNHG3 drives breast cancer progression by epigenetically increasing CSNK2A1 expression level
Zhenlin Nie1, Mu Xu1, Linpeng Zhou2
1Department of Laboratory Medicine, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, Jiangsu, China.
Small nucleolar RNA host gene 3 (SNHG3) drives breast cancer progression by regulating CSNK2A1. Inhibiting SNHG3 suppressed tumor growth, suggesting it as a potential diagnostic and therapeutic target for breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
- Aberrant expression of lncRNAs contributes to the initiation and progression of various cancers, including breast cancer.
Purpose of the Study:
- To investigate the role of small nucleolar RNA host gene 3 (SNHG3) in breast cancer progression.
- To elucidate the underlying molecular mechanisms by which SNHG3 influences breast cancer malignancy.
Main Methods:
- Analysis of RNA sequencing data from breast cancer tissues.
- In vitro and in vivo experiments including cell proliferation, apoptosis, and xenograft assays.
- Mechanistic studies involving bioinformatics, RNA fluorescence in situ hybridization, luciferase reporter assays, and RNA immunoprecipitation.
Main Results:
- SNHG3 expression was significantly upregulated in breast cancer tissues and correlated with poor patient survival.
- SNHG3 knockdown inhibited breast cancer cell proliferation and tumor growth in vitro and in vivo.
- SNHG3 was found to promote breast cancer progression by sponging miR-485-5p and upregulating Casein kinase II-A1 (CSNK2A1) expression in the cytoplasm.
Conclusions:
- SNHG3 acts as an oncogene in breast cancer, promoting malignant progression through the SNHG3/miR-485-5p/CSNK2A1 axis.
- SNHG3 represents a potential biomarker for breast cancer diagnosis and a promising therapeutic target.
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