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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

Zeitschrift:
BMC Cancer > Ausgabe 1/2018
Autoren:
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.

Abstract

Background

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.

Methods

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.

Results

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.

Conclusions

Upregulated miR-200a enhances treatment resistance via antagonizing TP53INP1 and YAP1 in breast cancer.
Zusatzmaterial
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)
12885_2017_3930_MOESM1_ESM.docx
Additional file 2: Fig. S1. Expression of p73 in MDA-MB-231 and MDA-MB-231 GR cells. (EPS 588 kb)
12885_2017_3930_MOESM2_ESM.eps
Literatur
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