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A PTAL-miR-101-FN1 Axis Promotes EMT and Invasion-Metastasis in Serous Ovarian Cancer
- Source :
- Molecular Therapy: Oncolytics, Vol 16, Iss , Pp 53-62 (2020)
- Publication Year :
- 2020
- Publisher :
- Elsevier, 2020.
-
Abstract
- Long non-coding RNAs (lncRNAs) play vital roles in the metastasis and invasion of cancer cells. Systematic analysis of ovarian cancer (OvCa) expression profiles suggests that deregulation of lncRNA AC004988.1, designated promoting transition-associated lncRNA (PTAL), is involved in OvCa progression. However, the underlying mechanism of PTAL in OvCa remains unknown. In this study, we showed that PTAL was significantly upregulated in mesenchymal subtype samples compared with epithelial subtype samples from TCGA serous OvCa datasets. PTAL expression was positively correlated with the expression of fibronectin1 (FN1), whereas PTAL and FN1 were negatively correlated with miR-101 expression in the mesenchymal OvCa samples. In addition, knockdown of PTAL inhibited cell migration and invasion and blunted the progression of metastasis in vitro. Meanwhile, knockdown of PTAL increased the expression of miR-101 and subsequently inhibited the expression of FN1. Importantly, PTAL positively regulated the expression of FN1 through sponging of miR-101 and promoted OvCa cell metastasis by regulating epithelial-mesenchymal transition. Overall, our study demonstrates the role of PTAL as a miRNA sponge in OvCa and suggests that PTAL may be a potential target for preventing OvCa metastasis. Keywords: ovarian cancer, epithelial-mesenchymal transition, lncRNA PTAL, miR-101, FN1
- Subjects :
- Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Subjects
Details
- Language :
- English
- ISSN :
- 23727705
- Volume :
- 16
- Issue :
- 53-62
- Database :
- Directory of Open Access Journals
- Journal :
- Molecular Therapy: Oncolytics
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.09a3a94ccad42bcb6cda3613df0888b
- Document Type :
- article
- Full Text :
- https://doi.org/10.1016/j.omto.2019.12.002