Publication: ET-1 Promotes Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells via the microRNA-489-3p /TWIST Axis
| cris.lastimport.scopus | 2026-03-12T16:02:23Z | |
| dc.creator | Tzeng, Huey-En | |
| dc.creator | Tang, Chih-Hsin | |
| dc.creator | Tsai, Chun-Hao | |
| dc.creator | Chiu, Chih-Hui | |
| dc.creator | Wu, Min-Huan | |
| dc.creator | Yen, Yun | |
| dc.date | 2021 | |
| dc.date.accessioned | 2021-11-08T07:23:03Z | |
| dc.date.accessioned | 2025-07-27T15:03:20Z | |
| dc.date.available | 2021-11-08T07:23:03Z | |
| dc.date.issued | 2021-11-08T07:23:03Z | |
| dc.description.abstract | Objective: Oral squamous cell carcinoma (OSCC) constitutes almost 90% of head and neck malignancies and has a poor prognosis. To improve the efficacy of OSCC therapy, it is of great significance to explore other therapy for OSCC. Endothelin-1 (ET-1), a potent vasoconstrictor peptide, is implicated in cancer pathogenesis. Moreover, ET-1 promotes epithelial-mesenchymal transition (EMT) during the development of human cancers. We further to found that ET-1 exposure induced EMT in human squamous cell carcinoma cell lines SCC4 and SAS, by enhancing the expression of EMT biomarkers N-cadherin and vimentin and reducing E-cadherin expression via upregulation of the transcription factor TWIST. Materials and Methods: Cell motility was examined by migration, invasion and wound healing assays. Quantitative real time polymerase chain reaction (q-PCR), and promoter assays confirmed the inhibitory effects of ET-1 on miRNAs expression in oral cancer cells. We demonstrate an intravenous injection model of lung metastasis followed by an advanced method for quantifying metastatic tumor using image analysis software. Results: In addition, ET-1/ETAR reduced levels of microRNA-489-3p (miR-489-3p), a transcriptional repressor of TWIST. We have identified a novel bypass mechanism through which ET-1/ETAR are involved in TWIST signaling and downregulate miR-489-3p expression, enabling OSCC cells to acquire the EMT phenotype. Notably, ET-1 knockdown dramatically decreased levels of EMT markers and cell migration potential. Conclusion: The role of ET-1 in OSCC progression is supported by our findings from an in vivo murine model of OSCC. ET-1 may therefore represent a novel molecular therapeutic in OSCC metastasis. | |
| dc.format.extent | 195 bytes | |
| dc.format.mimetype | text/html | |
| dc.identifier.doi | 10.2147/OTT.S294312 | |
| dc.identifier.issn | 1178-6930 | |
| dc.identifier.uri | https://ir.ntus.edu.tw/handle/987654321/64481 | |
| dc.language | en_US | |
| dc.publisher | NEW ZEALAND: DOVE MEDICAL PRESS | |
| dc.relation | ONCOTARGETS AND THERAPY, 14, p.5005-5018 | |
| dc.subject | oral squamous cell carcinoma | |
| dc.subject | endothelin-1 | |
| dc.subject | TWIST | |
| dc.subject | microRNA-489-3p | |
| dc.subject | epithelial-mesenchymal transition | |
| dc.title | ET-1 Promotes Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells via the microRNA-489-3p /TWIST Axis | |
| dc.type | article | |
| dspace.entity.type | Publication |