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MiR-548 K regulatory effect on the ABCG2 gene expression in MDR breast cancer cells
Mohammadreza Saberiyan1, Zahra Ghasemi2, Hajar Yaghoobi3
1Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Background:
multidrug resistance (MDR) is One of the foremost challenges in overcoming breast cancer. Various molecular processes are involved in the development of MDR in breast cancer cells, including over expression of ABC transporters such as ABCG2 (BCRP), increase breast cancer stem cells drug resistance, and epithelial mesenchymal transition.
Aims:
In the present study, we used bioinformatics and experimental analysis to investigate the role of miR-548 K, in the modulating of ABCG2, in MDR breast cancer cells.
Methods And Results:
In silico inspections introduce 14 microRNAs targeting 3'-UTR region of ABCG2 transcripts, which are probably involved in breast cancer drug resistance. An association was highlighted between miR-548 k with ABC transporter family. The expression level of ABCG2 gene in MCF7-MX cell lines was significantly more than MCF7 cell lines. On the other hand, we increased the expression of miR-548 K in MCF7-MX and MCF7 cell lines through its transfection, which dramatically coincided with decreasion in the ABCG2 transcripts level. Additional studies on patient samples revealed that the expression of ABCG2 showed an increase in ABCG2 level in neoadjuvant chemotherapy drugs resistance (NCDR) patients compared to primary pre-operative chemotherapy drugs response (PCDR) patients. Also, a reduction in the expression of miR-548 K in NCDR patients was revealed.
Conclusion:
The results of our study suggest that miR-548 K may be involved in modulating the expression of ABCG2 in MDR breast cancer cells.
Insights
This study reveals that miR-548K may regulate ABCG2 expression in multidrug-resistant (MDR) breast cancer. Lower miR-548K levels correlate with increased ABCG2, suggesting a role in chemotherapy resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Multidrug resistance (MDR) is a major obstacle in breast cancer treatment.
- Key mechanisms include ABC transporter overexpression (e.g., ABCG2), increased cancer stem cell resistance, and epithelial-mesenchymal transition.
Purpose of the Study:
- To investigate the role of miR-548K in modulating ABCG2 expression within MDR breast cancer cells.
- To explore the potential of miR-548K as a therapeutic target for overcoming drug resistance.
Main Methods:
- Bioinformatics analysis to identify microRNAs targeting ABCG2 3'-UTR.
- In vitro experiments involving transfection to alter miR-548K expression in breast cancer cell lines (MCF7 and MCF7-MX).
- Analysis of ABCG2 and miR-548K expression in patient samples with varying chemotherapy responses.
Main Results:
- In silico analysis identified 14 potential microRNA targets for ABCG2, with miR-548K showing a notable association.
- Increased miR-548K expression in MCF7-MX and MCF7 cells led to a significant decrease in ABCG2 transcripts.
- Elevated ABCG2 and reduced miR-548K expression were observed in patients resistant to neoadjuvant chemotherapy (NCDR) compared to those responding to primary chemotherapy (PCDR).
Conclusions:
- miR-548K plays a role in regulating ABCG2 expression in multidrug-resistant breast cancer.
- The findings suggest miR-548K could be a potential biomarker or therapeutic target for overcoming breast cancer MDR.
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