Key points are not available for this paper at this time.
Drug resistance in tumors is the primary contributor to clinical treatment failures, and aberrant expression of small RNA molecules, specifically microRNAs (miRNAs), in tumor tissues is intricately associated with drug resistance. The aim of this study is to investigate the targets and mechanisms through which exosomal miRNAs from triple-negative breast cancer (TNBC) regulate chemotherapy resistance in tumor cells. Utilizing high-throughput sequencing technology, we conducted exosomal miRNA sequencing on serum samples obtained from TNBC patients who were either sensitive or resistant to AC-sequential T chemotherapy. Subsequently, we identified and screened differentially expressed miRNAs. The observed differences in miRNA expression were further validated through quantitative reverse transcription-polymerase chain reaction. In comparison to TNBC patients who exhibited sensitivity to the AC-sequential T regimen chemotherapy, we identified significant differences in the expression of 85 miRNAs within serum exosomes of patients displaying chemotherapy resistance. Furthermore, we observed a substantial difference in the expression of hsa-miR-6831-5p between TNBC patients who were responsive to chemotherapy and those who were drug-resistant and underwent treatment with the AC-sequential T regimen. hsa-miR-6831-5p holds the potential to serve as a diagnostic marker for assessing the chemosensitivity of the AC-sequential T regimen in TNBC.
Building similarity graph...
Analyzing shared references across papers
Loading...
Le Yang
Jingjing Fan
Chao Dong
Medicine
Xinjiang Medical University
Tumor Hospital of Xinjiang Medical University
Building similarity graph...
Analyzing shared references across papers
Loading...
Yang et al. (Fri,) studied this question.
www.synapsesocial.com/papers/68e5a3eab6db64358753db3b — DOI: https://doi.org/10.1097/md.0000000000038549
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: