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Updated: Oct 26, 2025
Monitoring of Nanodrug Accumulation in Murine Breast Cancer Metastases
Published on: August 23, 2024
MiR-221 Expression Level Correlates with Insulin-Induced Doxorubicin Resistance in MCF-7 Breast Cancer Cells
Parisa Kheradmand1, Sadeq Vallian Boroojeni1, Saeed Esmaeili-Mahani2
1Department of Cellular and Molecular Biology and Microbology, Faculty of Science and Technology, University of Isfahan, Isfahan, Iran.
Objective:
Insulin induces anti-cancer drugs resistance in tumor cells. However, the mechanism by which insulin induces its drug resistance effects is not clear. In the present study, the expression of miR-221 in insulin-treated MCF-7 cells in response to the anti-cancer drug doxorubicin, was investigated.
Materials And Methods:
In this experimental study, cell viability was evaluated using MTT (3-[4,5 dimethylthiazol-2- yl]-2,5-diphenyl tetrazolium bromide) assay. The expression level of miR-221 was determined by real time polymerase chain reaction (RT-PCR). Furthermore, the expression of insulin receptor (IR) and cleaved caspase-3 protein was assessed by Western blotting.
Results:
The results showed that treatment of the MCF-7 cells with insulin reduced the anti-cancer effects of doxorubicin. Viability of naive and insulin-treated cells following doxorubicin (DOX) treatment was 62.9 ± 5.7% and 79 ± 7.2%, respectively. Furthermore, the expression of miR-221 in insulin-treated cells was significantly increased (2.6 ± 0.37-fold change) as compared with the control group. A significant decrease (26%) in the expression of caspase-3 protein and a significant increase (24%) in IR were observed in insulin-induced drug resistant MCF-7 cells as compared to the naive cells.
Conclusion:
Together, the data showed a positive correlation between the expression of miR-221 and IR expression, but a negative correlation with caspase3 expression, in insulin-induced drug resistant MCF-7 breast cancer cells. This could suggest a new mechanism for the role of miR-221 in cancer drugs resistance induced by insulin.
Insights
Insulin treatment increases miR-221 expression in breast cancer cells, promoting resistance to doxorubicin by upregulating the insulin receptor and downregulating caspase-3. This suggests a novel mechanism for insulin-induced drug resistance.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Insulin is known to induce anti-cancer drug resistance in tumor cells.
- The precise mechanisms underlying insulin's role in drug resistance remain unclear.
- This study investigates the involvement of microRNA-221 (miR-221) in insulin-mediated resistance.
Purpose of the Study:
- To investigate the expression of miR-221 in MCF-7 breast cancer cells treated with insulin and doxorubicin.
- To elucidate the role of miR-221 in insulin-induced resistance to chemotherapy.
- To explore the correlation between miR-221, insulin receptor (IR), and caspase-3 expression.
Main Methods:
- MCF-7 cells were treated with insulin and doxorubicin.
- Cell viability was assessed using the MTT assay.
- miR-221 expression was quantified via real-time PCR.
- Insulin receptor (IR) and cleaved caspase-3 protein levels were determined by Western blotting.
Main Results:
- Insulin treatment reduced the efficacy of doxorubicin, increasing cell viability.
- miR-221 expression was significantly upregulated in insulin-treated cells.
- Insulin-induced drug-resistant cells showed increased IR expression and decreased caspase-3 expression.
Conclusions:
- A positive correlation exists between miR-221 and IR expression, and a negative correlation with caspase-3.
- These findings suggest a novel mechanism involving miR-221 in insulin-induced breast cancer drug resistance.
- Targeting miR-221 may offer a strategy to overcome insulin-driven chemoresistance.
