Pathway study and systematic evaluation of microRNAs involved in anthracycline- induced cardiotoxicity in breast cancer patients
AbstractBackground Anthracycline treatment often causes cardiotoxicity in breast cancer patients. Imaging and cardiac biomarkers are now used as criteria for cardiotoxicity. However, new biomarkers are needed for early diagnosis. Gene expression may be controlled, in part, by little non-coding RNA molecules called microRNAs (miRNAs). Several microRNAs (miRNAs) have been linked to cardiovascular illness and are being studied as indicators for cardiotoxicity caused by cancer treatments. Methods We conducted a comprehensive search of the literature until April 2020 using the following databases: Medline/PubMed, Cochrane Central Register of Controlled Trials, Scopus, Lilacs, Web of Science, and Embase. Anthracycline-induced cardiotoxicity and non-cardiotoxicity patients with breast cancer who participated in cohort studies reporting miRNA biomarkers were considered. Moreover, we examined the miRTarBase for experimentally confirmed miRNA-target interactions. Results Only five of the 209 studies that were found met the requirements for inclusion. Two population-based cohorts confirmed the validity of Let-7f, miR-1, miR-20a, miR-126, and miR-210. Epirubicin-cardiotoxicity dramatically down-regulated the pro-angiogenic miRNAs let-7f, miR-20a, miR-126, and miR-210, compared to the non-cardiotoxicity group. Although alterations in miR-1 levels have been debated in doxorubicin-treated breast cancer patients with cardiotoxicity, they have been demonstrated to give diagnostic and prognostic information in the context of myocardial infarction. Target genes for let-7f, miR-1, miR-20a, miR-126, and miR-210 were used to compile a cardiotoxicity-related reactome pathway. Conclusion Anthracycline-based cardiotoxicity during breast cancer treatment seems to be linked to let-7f, miR-1, miR-20a, miR-126, and miR-210.