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Knockdown Of lncRNA NCK-AS1 Regulates Cisplatin Resistance Through Modulating miR-137 In Osteosarcoma Cells
Yi Cheng1,2, Xiaofei Shen2, Minqian Zheng2
1Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, People's Republic of China.
Purpose:
Long non-coding RNAs (lncRNAs) have been proved to act crucial parts in the progress of human tumor. However, the role of lncRNAs in drug resistance of tumor cells remains to be further elucidated. The present study aimed to explore whether lncRNA NCK-AS1 could affect the cisplatin (DDP) resistance in human osteosarcoma cell and the underlying molecular mechanism.
Methods:
The expression of NCK1-AS1 and miR-137 in osteosarcoma cells was detected by qRT-PCR. CCK-8 assay, colony formation assay, Western blotting, wound healing assay and transwell assay were employed to assess the cell proliferation, migration and invasion. In addition, CCK-8 assay, flow cytometry, qRT-PCR and resistance gene activity analysis were performed to assess the DDP sensitivity of osteosarcoma cells. The interaction between NCK1-AS1 and miR-137 was identified using a dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay.
Results:
The results revealed that NCK1-AS1 was significantly upregulated in osteosarcoma cells, as well as in DDP-resistant osteosarcoma cells. NCK1-AS1 silence inhibited the proliferation, migration and invasion of osteosarcoma cells, whereas enhanced the sensitivity of osteosarcoma cells to DDP. Furthermore, NCK1-AS1 directly interacted with miR-137 and overexpression of miR-137 suppressed the proliferation, migration and invasion of osteosarcoma cells. Most importantly, miR-137 overexpression enhanced the sensitivity of osteosarcoma cells to DDP, and high expression of NCK1-AS1 reversed the influences of miR-137 overexpression on DDP-resistant cells.
Conclusion:
In short, NCK1-AS1 knockdown enhanced DDP sensitivity of osteosarcoma cells by regulating miR-137, which may be a novel potential target for anti-DDP resistance in human osteosarcoma.
Insights
Long non-coding RNA NCK-AS1 promotes cisplatin resistance in osteosarcoma by downregulating miR-137. Silencing NCK-AS1 enhances drug sensitivity, offering a potential therapeutic target for osteosarcoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) play roles in tumor progression.
- The function of lncRNAs in tumor drug resistance requires further investigation.
Purpose of the Study:
- To investigate the role of lncRNA NCK-AS1 in cisplatin (DDP) resistance in human osteosarcoma.
- To elucidate the underlying molecular mechanism involving miR-137.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to detect NCK-AS1 and miR-137 expression.
- Cell proliferation, migration, invasion, and DDP sensitivity assays (CCK-8, colony formation, Western blotting, wound healing, Transwell, flow cytometry).
- Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm NCK-AS1 and miR-137 interaction.
Main Results:
- NCK-AS1 was upregulated in osteosarcoma and DDP-resistant cells.
- NCK-AS1 silence inhibited cell proliferation, migration, invasion, and increased DDP sensitivity.
- NCK-AS1 directly interacted with miR-137; miR-137 overexpression suppressed cell progression and enhanced DDP sensitivity.
- High NCK-AS1 expression reversed the effects of miR-137 overexpression in DDP-resistant cells.
Conclusions:
- NCK-AS1 knockdown enhances DDP sensitivity in osteosarcoma by regulating miR-137.
- NCK-AS1 may serve as a potential therapeutic target to overcome DDP resistance in osteosarcoma.
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