Abstract：
:Human breast cancers include cancer stem cell populations as well as nontumorigenic cancer cells. Breast cancer stem cells have self-renewal capability and are resistant to conventional chemotherapy. miRNAs regulate the expression of many target genes; therefore, dysregulation of miRNAs has been associated with the pathogenesis of human diseases, including cancer. However, a role for miRNA dysregulation in stemness and drug resistance has yet to be identified. Members of the miR34 family are reportedly tumor-suppressor miRNAs and are associated with various human cancers. Our results confirm that miR34a expression was downregulated in MCF7/ADR cells compared with MCF7 cells. We hypothesized that this reduction was due to the p53 (TP53) mutation in MCF7/ADR cells. In this study, we found that primary and mature miR34a were suppressed by treatment with p53 RNAi or the dominant-negative p53 mutant in MCF7 cells. Ectopic miR34a expression reduced cancer stem cell properties and increased sensitivity to doxorubicin treatment by directly targeting NOTCH1. Furthermore, tumors from nude mice treated with miR34a were significantly smaller compared with those of mice treated with control lentivirus. Our research suggests that the ectopic expression of miR34a represents a novel therapeutic approach in chemoresistant breast cancer treatment.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Park EY,Chang E,Lee EJ,Lee HW,Kang HG,Chun KH,Woo YM,Kong HK,Ko JY,Suzuki H,Song E,Park JHdoi
10.1158/0008-5472.CAN-14-1140subject
Has Abstractpub_date
2014-12-15 00:00:00pages
7573-82issue
24eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-14-1140journal_volume
74pub_type
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