Long noncoding RNA ATB promotes the epithelial-mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer.
Rong-Hui LiMin ChenJing LiuChang-Chun ShaoCui-Ping GuoXiao-Long WeiYao-Chen LiWen-He HuangGuo-Jun ZhangPublished in: Cell death & disease (2018)
Recent 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.
Keyphrases
- epithelial mesenchymal transition
- long noncoding rna
- poor prognosis
- cell migration
- transforming growth factor
- free survival
- long non coding rna
- signaling pathway
- breast cancer cells
- case control
- high glucose
- lymph node
- squamous cell carcinoma
- diabetic rats
- endothelial cells
- radiation therapy
- atomic force microscopy
- neoadjuvant chemotherapy