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01.12.2018 | Research article | Ausgabe 1/2018 Open Access

BMC Cancer 1/2018

MicroRNA-200a confers chemoresistance by antagonizing TP53INP1 and YAP1 in human breast cancer

BMC Cancer > Ausgabe 1/2018
San-Jian Yu, Liu Yang, Qi Hong, Xia-Ying Kuang, Gen-Hong Di, Zhi-Ming Shao
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1186/​s12885-017-3930-0) contains supplementary material, which is available to authorized users.



Emerging evidence suggests molecular and phenotypic association between treatment resistance and epithelial–mesenchymal transition (EMT) in cancer. Compared with the well-defined molecular events of miR-200a in EMT, the role of miR-200a in therapy resistance remains to be elucidated.


Breast cancer cells transfected with mimic or inhibitor for miR-200a was assayed for chemoresistance in vitro. miR-200a expression was assessed by quantitative real-time PCR (qRT-PCR) in breast cancer patients treated with preoperative chemotherapy. Luciferase assays, cell proliferation assay were performed to identify the targets of miR-200a and the mechanism by which it promotes treatment resistance. Survival analysis was used to evaluate the prognosis value of miR-200a.


In this study, our results showed ectopic expression of miR-200a promotes chemoresistance in breast cancer cell lines to several chemotherapeutic agents, whereas inhibition of miR-200a enhances gemcitabine chemosensitivity in resistance cancer cells. We found overexpression of miR-200a was closely associated with poor response to preoperative chemotherapy and poor prognosis in breast cancer patients. Furthermore, knockdown of YAP1 and TP53INP1 phenocopied the effects of miR-200a overexpression, and confirmed that TP53INP1 is a novel target of miR-200a. Remarkably, TP53INP1 expression is inversely correlated with miR-200a expression in Breast cancer cell lines. Taken together, these clinical and experimental results demonstrate that miR-200a is a determinant of chemoresistance of breast cancer.


Upregulated miR-200a enhances treatment resistance via antagonizing TP53INP1 and YAP1 in breast cancer.
Additional file 1: Table S1. List of primer and siRNA sequences. Table S2: Intersection between predict target of miR-200a and p53 family binding partner. (DOCX 17 kb)
Additional file 2: Fig. S1. Expression of p73 in MDA-MB-231 and MDA-MB-231 GR cells. (EPS 588 kb)
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