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Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the
Yuan Wang1, Li Zhang2, Xifu Zheng1
1Department of Orthopaedics, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116044, China.
Abstract:
Chemotherapeutic insensitivity remains a major obstacle to osteosarcoma treatment. Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) play an essential role in tumourigenesis. However, the potential biological roles and regulatory mechanisms of novel lncRNAs in response to cisplatin treatment are poorly understood. Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway. Thus, these findings demonstrate that LINC00161 is an essential regulator in cisplatin-induced apoptosis, and the LINC00161-miR-645-IFIT2 signalling axis plays an important role in reducing osteosarcoma chemoresistance.
Insights
Long non-coding RNA LINC00161 enhances cisplatin effectiveness in osteosarcoma by promoting apoptosis. It targets miR-645, upregulating IFIT2 and overcoming chemoresistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Chemotherapeutic insensitivity is a significant challenge in osteosarcoma treatment.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in tumorigenesis.
- The function of novel lncRNAs in response to chemotherapy, like cisplatin, is not well understood.
Purpose of the Study:
- To investigate the role of lncRNA LINC00161 in osteosarcoma cells treated with cisplatin.
- To elucidate the molecular mechanisms by which LINC00161 affects chemoresistance.
- To identify potential therapeutic targets for overcoming cisplatin resistance in osteosarcoma.
Main Methods:
- Osteosarcoma cell lines were treated with cisplatin to assess LINC00161 expression.
- Functional assays were performed to evaluate the impact of LINC00161 on apoptosis and chemoresistance.
- Mechanistic studies, including RNA immunoprecipitation and luciferase reporter assays, were used to explore the interaction between LINC00161, miR-645, and IFIT2.
Main Results:
- LINC00161 expression was induced by cisplatin in osteosarcoma cells.
- Overexpression of LINC00161 enhanced cisplatin-induced apoptosis and reversed cisplatin resistance.
- LINC00161 was found to sponge miR-645, inhibiting its activity and leading to increased IFIT2 expression.
- The LINC00161-miR-645-IFIT2 pathway was identified as crucial for LINC00161's effect on apoptosis.
Conclusions:
- LINC00161 acts as a key regulator in cisplatin-induced apoptosis in osteosarcoma.
- The LINC00161-miR-645-IFIT2 signaling axis plays a critical role in reducing osteosarcoma chemoresistance.
- LINC00161 represents a potential therapeutic target for improving osteosarcoma treatment outcomes.
