| First Author | Saxena M | Year | 2021 |
| Journal | J Cell Sci | Volume | 134 |
| Issue | 21 | PubMed ID | 34633031 |
| Mgi Jnum | J:320566 | Mgi Id | MGI:6874467 |
| Doi | 10.1242/jcs.258418 | Citation | Saxena M, et al. (2021) The long non-coding RNA ET-20 mediates EMT by impairing desmosomes in breast cancer cells. J Cell Sci 134(21):jcs258418 |
| abstractText | The vast majority of breast cancer-associated deaths are due to metastatic spread of cancer cells, a process aided by epithelial-to-mesenchymal transition (EMT). Mounting evidence has indicated that long non-coding RNAs (lncRNAs) also contribute to tumor progression. We report the identification of 114 novel lncRNAs that change their expression during TGFbeta-induced EMT in murine breast cancer cells (referred to as EMT-associated transcripts; ETs). Of these, the ET-20 gene localizes in antisense orientation within the tenascin C (Tnc) gene locus. TNC is an extracellular matrix protein that is critical for EMT and metastasis formation. Both ET-20 and Tnc are regulated by the EMT master transcription factor Sox4. Notably, ablation of ET-20 lncRNA effectively blocks Tnc expression and with it EMT. Mechanistically, ET-20 interacts with desmosomal proteins, thereby impairing epithelial desmosomes and promoting EMT. A short transcript variant of ET-20 is shown to be upregulated in invasive human breast cancer cell lines, where it also promotes EMT. Targeting ET-20 appears to be a therapeutically attractive lead to restrain EMT and breast cancer metastasis in addition to its potential utility as a biomarker for invasive breast cancer. |
