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Knockdown of long non-coding RNA LINC00152 increases cisplatin sensitivity in ovarian cancer cells
1Department of Obstetrics and Gynecology, Beijing Shijitan Hospital of Capital Medical University, Beijing 100038, P.R. China.
Abstract:
Drug resistance severely limits the effectiveness of chemotherapeutic treatment in ovarian cancer. The present study aimed to investigate the role of long non-coding RNA LINC00152 (LINC00152) in the cisplatin resistance of ovarian cancer. The expression level of LINC00152 was significantly increased in the ovarian cancer CoC1 and CoC1/DDP cell lines compared with the normal ovarian IOSE-80 cell line. To further investigate the function of LINC00152, small interfering RNAs (siRNAs) targeting LINC00152 were transfected into COC1 and COC1/DDP cells, which were subsequently treated with varying concentrations of cisplatin. The results revealed that LINC00152 silencing increased the apoptotic rates and enhanced the chemosensitivity of CoC1 and CoC1/DDP cells to cisplatin. Furthermore, downregulation of LINC00152 significantly decreased Bcl-2, and increased Bax and cleaved caspase-3 expression levels. Additionally, LINC00152 silencing decreased the expression of multidrug resistance-associated gene 1 (MDR1), multidrug resistance-associated protein 1 (MRP1) and glutathione S-transferase π (GSTπ). Collectively, the data demonstrated that LINC00152 knockdown increased the chemosensitivity of epithelial ovarian cancer cells to cisplatin by increasing apoptosis and decreasing the expression levels of MDR1, MRP1 and GSTπ.
Insights
Long non-coding RNA LINC00152 promotes cisplatin resistance in ovarian cancer. Silencing LINC00152 increases cancer cell sensitivity to chemotherapy by enhancing apoptosis and reducing drug resistance markers.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Drug resistance is a major challenge in ovarian cancer chemotherapy.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression and treatment resistance.
Purpose of the Study:
- To investigate the role of long non-coding RNA LINC00152 in cisplatin resistance in ovarian cancer.
- To explore the underlying mechanisms by which LINC00152 influences chemosensitivity.
Main Methods:
- Quantitative analysis of LINC00152 expression in ovarian cancer cell lines.
- Transfection of small interfering RNAs (siRNAs) to silence LINC00152 in ovarian cancer cells.
- Assessment of cell apoptosis, chemosensitivity, and expression of key proteins (Bcl-2, Bax, cleaved caspase-3) and drug resistance genes (MDR1, MRP1, GSTπ) following LINC00152 knockdown.
Main Results:
- LINC00152 expression was significantly elevated in cisplatin-resistant ovarian cancer cells.
- Silencing LINC00152 enhanced cisplatin-induced apoptosis and chemosensitivity.
- Downregulation of LINC00152 led to decreased Bcl-2 and increased Bax and cleaved caspase-3 levels.
- LINC00152 knockdown reduced the expression of multidrug resistance genes MDR1, MRP1, and GSTπ.
Conclusions:
- LINC00152 plays a crucial role in conferring cisplatin resistance in epithelial ovarian cancer.
- Targeting LINC00152 represents a potential therapeutic strategy to overcome drug resistance in ovarian cancer.
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