Article Publish Status: FREE
Abstract Title:

Shikonin reduces tamoxifen resistance through long non-coding RNA uc.57.

Abstract Source:

Oncotarget. 2017 Oct 24 ;8(51):88658-88669. Epub 2017 Sep 11. PMID: 29179465

Abstract Author(s):

Chen-Han Zhang, Jue Wang, Lin-Xin Zhang, Yi-Han Lu, Tian-Hao Ji, Lu Xu, Li-Jun Ling

Article Affiliation:

Chen-Han Zhang


Tamoxifen resistance is a serious problem in the endocrine therapy of breast cancer. Long non-coding RNAs play important roles in tumor development. In this study, we revealed the involvement of lncRNA uc.57 and its downstream gene BCL11A in TAM resistance. Tamoxifen-resistant MCF-7R cells showed lower expression of uc.57 and higher expression of BCL11A mRNA and protein than the parental MCF-7 cells. Moreover, levels of uc.57 mRNA were lower and BCL11A mRNA were higher in breast cancer tissues than in precancerous breast tissues. Shikonin treatment reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo, targeting uc.57/BCL11A. Fluorescence in situ hybridization and RNA immunoprecipitation analyses showed that uc.57 binds to BCL11A. Uc.57 overexpression downregulated BCL11A and reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo. BCL11A knockdown also reduced tamoxifen resistance by inhibiting PI3K/AKT and MAPK signaling pathways. It thus appears shikonin reduces tamoxifen resistance of MCF-7R breast cancer cells by inducing uc.57, which downregulates BCL11A to inhibit PI3K/AKT and MAPK signaling pathways.

Study Type : In Vitro Study

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