Long noncoding RNA ATB promotes the epithelial−mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer

Adult 0301 basic medicine Epithelial-Mesenchymal Transition Mice, Nude Nuclear Proteins Breast Neoplasms Middle Aged Prognosis Article 3. Good health Cohort Studies Gene Expression Regulation, Neoplastic Mice MicroRNAs 03 medical and health sciences Cell Movement Lymphatic Metastasis MCF-7 Cells Animals Humans Female Neoplasm Invasiveness Cell Proliferation Neoplasm Staging
DOI: 10.1038/s41419-018-1210-9 Publication Date: 2018-12-05T09:55:30Z
ABSTRACT
AbstractRecent studies indicate that the long noncoding RNA ATB (lncATB) can induce the epithelial−mesenchymal transition (EMT) in cancer cells, but the specific cellular targets of lncATB require further investigation. In the present study, the upregulation of lncATB in breast cancer cells was validated in a TGF-β-induced EMT model. Gain- and loss-of-function studies demonstrated that lncATB enhanced cell migration, invasion and clonogenicity in vitro and in vivo. LncATB promoted the EMT by acting as a sponge for the miR-200 family and restoring Twist1 expression. Subsequently, the clinical significance of lncATB was investigated in a cohort of breast cancer patients (N = 131). Higher lncATB expression was correlated with increased nodal metastasis (P = 0.036) and advanced clinical stage (P = 0.011) as well as shorter disease-free survival (P = 0.043) and overall survival (P = 0.046). These findings define Twist1 as a major target of lncATB in the induction of the EMT and highlight lncATB as a biomarker in breast cancer patients.
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