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SNHG15 Contributes To Cisplatin Resistance In Breast Cancer Through Sponging miR-381
Hailong Mi1, Xiaochun Wang1, Fang Wang1
1Department of Breast Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 475000, People's Republic of China.
Background:
Increasing evidence implies the participation of long non-coding RNAs (lncRNAs) in chemoresistance to cancer treatment. Their role and molecular mechanisms in breast cancer chemoresistance, nevertheless, are yet not considerably elucidated. In this work, we research the function of small nucleolar RNA host gene 15 (SNHG15) in cisplatin (DDP) resistance of breast cancer and uncover the underlying molecular mechanism.
Methods:
SNHG15 and miR-381 expression levels were detected using Quantitative real-time PCR (qRT-PCR) analysis. The functional roles of SNHG15 and miR-381 in breast cancer were determined using MTT assay and flow cytometry analysis. The effect of SNHG15 on miR-381 expression was determined using Luciferase reporter assay, RNA immunoprecipitation (RIP) assay and qRT-PCR analysis.
Results:
SNHG15 was found to be up-regulated in cisplatin resistant breast cancer tissues and cell lines. Breast cancer patients with high SNHG15 expression had a poor prognosis. SNHG15 silencing enhanced cisplatin sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. Additionally, SNHG15 could function as a miR-381 sponge. miR-381 overexpression could overcome cisplatin resistance. miR-381 knockdown countered SNHG15 knockdown-mediated enhancement of cisplatin sensitivity in MCF-7/DDP and MDA-MB-231/DDP cells. Besides, SNHG15 knockdown facilitated cisplatin sensitivity of cisplatin resistant breast cancer cells in vivo.
Conclusion:
In summary, SNHG15 knockdown overcame cisplatin resistance of breast cancer by sponging miR-381, providing a novel therapeutic target for breast cancer.
Insights
Small nucleolar RNA host gene 15 (SNHG15) promotes cisplatin resistance in breast cancer by sponging miR-381. Silencing SNHG15 enhances chemoresistance, offering a new therapeutic target for breast cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly implicated in cancer treatment chemoresistance.
- The specific roles and mechanisms of lncRNAs in breast cancer chemoresistance remain underexplored.
- This study investigates the function of small nucleolar RNA host gene 15 (SNHG15) in cisplatin resistance in breast cancer.
Purpose of the Study:
- To elucidate the role of SNHG15 in cisplatin resistance in breast cancer.
- To uncover the molecular mechanism by which SNHG15 influences chemoresistance.
- To evaluate SNHG15 as a potential therapeutic target for overcoming cisplatin resistance.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) was used to measure SNHG15 and miR-381 expression.
- Functional assays including MTT and flow cytometry assessed the roles of SNHG15 and miR-381.
- Luciferase reporter, RNA immunoprecipitation (RIP), and qRT-PCR assays investigated the interaction between SNHG15 and miR-381.
Main Results:
- SNHG15 was upregulated in cisplatin-resistant breast cancer tissues and cell lines, correlating with poor patient prognosis.
- SNHG15 silencing increased cisplatin sensitivity in resistant cell lines (MCF-7/DDP, MDA-MB-231/DDP) both in vitro and in vivo.
- SNHG15 acted as a miR-381 sponge, and miR-381 overexpression or knockdown modulated cisplatin resistance, confirming the SNHG15/miR-381 axis.
Conclusions:
- SNHG15 knockdown effectively overcomes cisplatin resistance in breast cancer by sponging miR-381.
- The SNHG15/miR-381 interaction presents a novel molecular mechanism driving chemoresistance.
- Targeting SNHG15 offers a promising therapeutic strategy for enhancing breast cancer treatment efficacy.

