Literature DB >> 29258115

MiR-129-5p Sensitizes the Response of Her-2 Positive Breast Cancer to Trastuzumab by Reducing Rps6.

Xiangdong Lu1, Jingjing Ma2, Jiahui Chu3, Qing Shao1, Yao Zhang1, Guangping Lu3, Jun Li3, Xiang Huang3, Wei Li3, Yongfei Li3, Yang Ling4, Tao Zhao1,4.   

Abstract

BACKGROUND/AIMS: Trastuzumab is an important treatment used for patients with Her-2-positive breast cancer, but an increasing incidence of trastuzumab resistance has been observed clinically during the past decade. Aberrant microRNA (miR) expression levels are correlated with prognosis and response to trastuzumab in breast cancer. MiR-129-5p is downregulated in trastuzumab-resistant human breast cancer cells (JIMT-1), but its potential function and underlying mechanism remain unclear.
METHODS: Quantitative RT-PCR (qRT-PCR) was used to determine the expression levels of miR-129-5p and its potential target genes. The effects of miR-129-5p on cell responses to trastuzumab were analyzed by CCK-8 and flow cytometry assays in Her-2-positive breast cancer cells (SKBR-3 and JIMT-1). Bio-informatics analyses were performed to predict target genes of miR-129-5p, and luciferase assays were carried out to confirm the binding of miR-129-5p and rpS6.
RESULTS: MiR-129-5p, which was downregulated and predicted to target rpS6 in trastuzumab-resistant breast cancer cells, enhanced the sensitivity of breast cancer cells to trastuzumab by reducing the expression of rpS6. Moreover, the overexpression of rpS6 reversed the sensitivity of cells to trastuzumab induced by miR-129-5p.
CONCLUSIONS: MiR-129-5p sensitized Her-2-positive breast cancer to trastuzumab by downregulating rpS6. These findings provide novel insights into the common role of rpS6 and its related molecular mechanisms in mediating trastuzumab-resistance in Her-2-positive breast cancers.
© 2017 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Her-2-positive breast cancer; MiR-129-5p; RpS6; Trastuzumab resistance

Mesh:

Substances:

Year:  2017        PMID: 29258115     DOI: 10.1159/000486122

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  13 in total

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