1. LncRNA ZFAS1 promotes proliferation and migration and inhibits apoptosis in nasopharyngeal carcinoma via the PI3K/AKT pathway in vitro.
- Author
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Wang X, Jin Q, Wang X, Chen W, and Cai Z
- Subjects
- Biomarkers, Tumor genetics, Biomarkers, Tumor metabolism, Cell Cycle, Gene Expression Regulation, Neoplastic, Humans, In Vitro Techniques, Nasopharyngeal Carcinoma genetics, Nasopharyngeal Carcinoma metabolism, Nasopharyngeal Neoplasms genetics, Nasopharyngeal Neoplasms metabolism, Nasopharyngeal Neoplasms pathology, Phosphatidylinositol 3-Kinases genetics, Prognosis, Proto-Oncogene Proteins c-akt genetics, Tumor Cells, Cultured, Apoptosis, Cell Movement, Cell Proliferation, Nasopharyngeal Carcinoma pathology, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, RNA, Long Noncoding genetics
- Abstract
Background: Increasing evidence shows that long non-coding RNAs (lncRNAs) play a key role in the development of various cancers. Zinc finger antisense 1 (ZFAS1) is a novel lncRNA with previously demonstrated associations with several types of cancer. Here we examined the expression and potential function of the ZFAS1 in nasopharyngeal carcinoma (NPC)., Methods: We detected ZFAS1 expression in GSE12452, a human microarray dataset, and NPC cell lines. Small interfering RNA against ZFAS1 was used to elucidate the cellular functions of ZFAS1 using MTT, colony formation, cell cycle, cell apoptosis, transwell invasion and migration and western blot assays. An activator of the PI3K/AKT signaling pathway (740Y-P) was used to determine the contribution of PI3K/AKT., Results: ZFAS1 was significantly upregulated in NPC tissues and cell lines. Silencing ZFAS1 significantly inhibited cell proliferation and invasion, arrested cell cycle progression and promoted cell apoptosis, as well as reduced epithelial-mesenchymal transition. Moreover, 740Y-P could rescue the effects of ZFAS1 knockdown on proliferation, apoptosis and invasion in 5-8F cells., Conclusions: ZFAS1 might play an oncogenic role in NPC and facilitate cell proliferation and invasion via the PI3K/AKT signaling pathway in NPC cells.
- Published
- 2019
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