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Knockdown of miR-182 changes the sensitivity of triple-negative breast cancer cells to cisplatin
Hülya Dönmez1, Bahadır Batar2, Burhan Turgut3
1Bone Marrow Transplant Unit, Medical Faculty, Tekirdağ Namık Kemal University, Tekirdağ, Turkey.
Abstract:
Breast cancer is the most common malignancy that affects women. MicroRNAs (miRNAs) play an essential role in cancer therapy and regulate many biological processes such as cisplatin resistance. The study's objective was to determine whether miR-182 dysregulation was the cause of cisplatin resistance in TNBC cell line MDA-MB-231. To determine the expression of miR-182, PCR was performed with primers specific to miR-182, and agarose gel electrophoresis was performed. To reduce the expression of miR-182 in MDA-MB-231 cells, anti-miR-182 oligonucleotides were used. RT-qPCR was used to confirm knockdown. The knockdown and control groups were treated with cisplatin at the same time. Propidium iodide (PI) and Annexin V staining were performed for apoptosis assay. Flow cytometric analysis was used to investigate the effect of miR-182 knockdown on cell cycle arrest. In comparison to untreated control MDA-MB-231 cells with MDA-MB-231 cells treated with anti-miR-182, there was a significant increase in the cisplatin-induced early apoptosis phase (p = 0.023). Also, inhibition of miR-182 significantly increased the cell cycle arrest at the G2/M phase in MDA-MB-231 cells (p = 0.031). Our results revealed that miR-182 inhibition may play a role in the overcoming of cisplatin resistance by inducing apoptosis and, cell cycle arrest in TNBC.
Insights
Inhibiting miR-182 in triple-negative breast cancer (TNBC) cells increased apoptosis and cell cycle arrest, potentially overcoming cisplatin resistance. This finding offers a new therapeutic strategy for TNBC treatment.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Breast cancer is a leading cause of cancer-related mortality in women.
- MicroRNAs (miRNAs) are critical regulators of biological processes, including chemoresistance.
- Cisplatin resistance is a significant challenge in treating triple-negative breast cancer (TNBC).
Purpose of the Study:
- To investigate the role of miR-182 dysregulation in cisplatin resistance in the TNBC cell line MDA-MB-231.
- To determine if inhibiting miR-182 can sensitize TNBC cells to cisplatin treatment.
Main Methods:
- Quantitative PCR (qPCR) and agarose gel electrophoresis were used to determine miR-182 expression.
- Anti-miR-182 oligonucleotides were employed to inhibit miR-182 expression in MDA-MB-231 cells.
- Apoptosis assays (Annexin V/Propidium Iodide staining) and flow cytometry were utilized to assess cell death and cell cycle arrest.
Main Results:
- Inhibition of miR-182 significantly increased cisplatin-induced apoptosis in MDA-MB-231 cells (p=0.023).
- Knockdown of miR-182 led to a significant increase in G2/M phase cell cycle arrest (p=0.031).
- These findings suggest miR-182 plays a role in conferring cisplatin resistance in TNBC.
Conclusions:
- Inhibiting miR-182 demonstrates potential in overcoming cisplatin resistance in triple-negative breast cancer.
- miR-182 inhibition induces apoptosis and cell cycle arrest, offering a promising therapeutic avenue for TNBC.
- Further research into miR-182 targeted therapies could improve treatment outcomes for TNBC patients.
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