Open AccessLong non‐coding RNA FTH 1P3 activates paclitaxel resistance in breast cancer through miR‐206/ ABCB 1
Author(s) -
Wang Ruoming,
Zhang Tengteng,
Yang Zhen,
Jiang Chunxia,
Seng Jingjing
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13679
Subject(s) - paclitaxel , gene silencing , breast cancer , microrna , cancer research , long non coding rna , biology , downregulation and upregulation , chemistry , cancer , gene , biochemistry , genetics
Emerging evidence has indicated the important function of long non‐coding RNA s (lnc RNA s) in tumour chemotherapy resistance. However, the underlying mechanism is still ambiguous. In this study, we investigate the physiopathologic role of lnc RNA ferritin heavy chain 1 pseudogene 3 ( FTH 1P3) on the paclitaxel ( PTX ) resistance in breast cancer. Results showed that lnc RNA FTH 1P3 was up‐regulated in paclitaxel‐resistant breast cancer tissue and cells ( MCF ‐7/ PTX and MDA ‐ MB ‐231/ PTX cells) compared with paclitaxel‐sensitive tissue and parental cell lines ( MCF ‐7, MDA ‐ MB ‐231). Gain‐ and loss‐of‐function experiments revealed that FTH 1P3 silencing decreased the 50% inhibitory concentration ( IC 50) value of paclitaxel and induced cell cycle arrest at G2/M phase, while FTH 1P3‐enhanced expression exerted the opposite effects. In vivo, xenograft mice assay showed that FTH 1P3 silencing suppressed the tumour growth of paclitaxel‐resistant breast cancer cells and ABCB 1 protein expression. Bioinformatics tools and luciferase reporter assay validated that FTH 1P3 promoted ABCB 1 protein expression through targeting miR‐206, acting as a mi RNA “sponge.” In summary, our results reveal the potential regulatory mechanism of FTH 1P3 on breast cancer paclitaxel resistance through miR‐206/ ABCB 1, providing a novel insight for the breast cancer chemoresistance.