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Published on: April 6, 2012
lncRNA GAS5-promoted apoptosis in triple-negative breast cancer by targeting miR-378a-5p/SUFU signaling
Shipeng Zheng1, Mengquan Li1, Keke Miao1
1Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Purpose:
Long-chain noncoding RNAs (lncRNAs) are involved in regulating the sensitivity of cancer cells to chemotherapeutic drugs, but the specific mechanism of action is not well understood. The aim of this study was to investigate the effect of lncRNA growth-stasis specific transcript 5 (GAS5) on triple-negative breast cancer (TNBC).
Methods:
Quantitative real-time polymerase chain reaction and flow cytometry were used to screen lncRNA associated with tumor resistance. Double luciferase reporter gene assay, flow cytometry, and Western blot assay were used to determine whether miRNA 378a-5p and SUFU were involved in tumor cell apoptosis induced by lncRNA GAS5. A mouse model of subcutaneous xenografts was established to investigate the relationship between lncRNA GAS5 and tumor resistance in vivo.
Results:
In this study, the expression of lncRNA GAS5 was significantly downregulated in cells treated with paclitaxel (PTX) or cisplatin (CIS). Furthermore, TNBC cells with low expression of lncRNA GAS5 had a lower percentage of apoptosis under stress conditions, especially in serum-free medium. More interestingly, the expression level of lncRNA GAS5 in TNBC patients was associated with tumor resistance to PTX and CIS. In addition, RNA immunoprecipitation experiments confirmed that lncRNA GAS5 and miR-378 could directly bind to each other. Moreover, the miR-378a-5p target of SUFU could promote lncRNA GAS5-induced apoptosis of TNBC cells. Finally, lncRNA GAS5 overexpressed MDA-231R could enhance the sensitivity of TNBC to PTX.
Conclusion:
The above results confirmed that lncRNA GAS5 could induce apoptosis in TNBC cells by targeting miR-378a-5p/SUFU signaling.
Insights
Long-chain noncoding RNA GAS5 (growth-stasis specific transcript 5) induces apoptosis in triple-negative breast cancer cells. This lncRNA targets miR-378a-5p/SUFU signaling, enhancing sensitivity to chemotherapy drugs like paclitaxel and cisplatin.
Area of Science:
- * Molecular biology
- * Cancer research
- * RNA biology
Background:
- * Long-chain noncoding RNAs (lncRNAs) influence cancer cell drug sensitivity.
- * The precise mechanisms of lncRNA action in chemotherapy resistance remain unclear.
- * Triple-negative breast cancer (TNBC) presents unique challenges in treatment.
Purpose of the Study:
- * To investigate the role of lncRNA growth-stasis specific transcript 5 (GAS5) in triple-negative breast cancer (TNBC).
- * To elucidate the mechanism by which GAS5 affects chemotherapy sensitivity in TNBC.
Main Methods:
- * Quantitative real-time PCR and flow cytometry for lncRNA screening.
- * Luciferase reporter assays, flow cytometry, and Western blot to assess apoptosis.
- * In vivo studies using a mouse xenograft model to evaluate tumor resistance.
Main Results:
- * GAS5 expression was downregulated in TNBC cells treated with paclitaxel or cisplatin.
- * Low GAS5 expression correlated with reduced apoptosis and increased chemoresistance in TNBC.
- * GAS5 directly binds to miR-378a-5p, and the miR-378a-5p/SUFU pathway promotes GAS5-induced apoptosis.
- * Overexpression of GAS5 enhanced TNBC sensitivity to paclitaxel in vivo.
Conclusions:
- * lncRNA GAS5 induces apoptosis in TNBC cells.
- * GAS5 exerts its function by targeting the miR-378a-5p/SUFU signaling pathway.
- * GAS5 represents a potential therapeutic target for overcoming chemoresistance in TNBC.
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