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AFAP1-AS1 Promotes Epithelial-Mesenchymal Transition and Tumorigenesis Through Wnt/β-Catenin Signaling Pathway in Triple-Negative Breast Cancer
Author(s) -
Kaiming Zhang,
Peng Liu,
Hailin Tang,
Xiaoming Xie,
Yanan Kong,
Cailu Song,
Xingsheng Qiu,
Xiangsheng Xiao
Publication year - 2018
Publication title -
frontiers in pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.384
H-Index - 86
ISSN - 1663-9812
DOI - 10.3389/fphar.2018.01248
Subject(s) - wnt signaling pathway , cancer research , carcinogenesis , triple negative breast cancer , epithelial–mesenchymal transition , downregulation and upregulation , catenin , breast cancer , cell growth , biology , tumor progression , cancer , signal transduction , microbiology and biotechnology , gene , biochemistry , genetics
Long non-coding RNA (LncRNA) actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) is overexpressed in various types of cancers and plays an important role in tumor progression and prognosis. This study investigates the role of AFAP1-AS1 in tumor progression in triple-negative breast cancer (TNBC). We found that AFAP1-AS1 was overexpressed in TNBC tissues and cells. Overexpression of LncRNA AFAP1-AS1 was associated with poor prognosis in TNBC patients. Moreover, we demonstrated that upregulation of AFAP1-AS1 promoted cell proliferation and invasion, and inhibited cell apoptosis in vitro , while overexpression of AFAP1-AS1 promoted tumor growth in vivo . Our results also revealed that upregulation of AFAP1-AS1 activated Wnt/β-catenin pathway to promote tumorigenesis and cell invasion by increasing the expression of C-myc and epithelial-mesenchymal transition-related molecules in TNBC. Collectively, AFAP1-AS1 can be an independent prognostic marker and an effective therapeutic target of triple- negative breast cancer.

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