The biological function of long noncoding RNA FAL1 in oesophageal carcinoma cells. Issue 1 (4th December 2019)

• Record Type: Journal Article
• Authors: Yang, Zhiguo; Liu, Dongyan; Wu, Dan; Liu, Fang; Liu, Cuiping
• Is Part Of: Artificial cells, nanomedicine, and biotechnology. Volume 47:Issue 1(2019)
• Page Start: 896
• Page End: 903
• Publication Date: 2019-12-04
• Subjects: Long non-coding RNAs -- FAL1 -- oesophageal squamous cell carcinoma -- cell proliferation; Artificial cells -- Periodicals; Nanotechnology -- Periodicals; Blood substitutes -- Periodicals; Tissue engineering -- Periodicals; Molecules -- Periodicals; Biotechnology -- Periodicals; 615.39
• DOI: 10.1080/21691401.2019.1573738
• Languages: English
• ISSNs: 2169-1401

Abstract

Abstract: Long non-coding RNAs (lncRNAs) have been reported to be involved in the pathogenesis of a variety of malignancies, including oesophageal cancer. Alterations of the lncRNA focally amplified lncRNA on chromosome 1 (FAL1) are present in epithelial tumours. However, its expression pattern and function in oesophageal cancer are poorly addressed. In the current study, we reported that FAL1 is upregulated in oesophageal cancer tissues and is positively correlated with outcomes in oesophageal squamous cell carcinoma (OSCC). Consecutive experiments revealed that the expression level of FAL1 is higher in OSCC cell lines than in human normal oesophageal epithelium cell line HEEpiCs. Importantly, Knockdown of FAL1 suppressed cell proliferation, increased cell cycle arrest, inhibited cell invasion and epithelial-mesenchymal transition (EMT) by affected related genes. In contrast, overexpression of FAL1 has the opposite effects. Our findings underline a novel biological mechanism in which FAL1 acts as a regulator of oesophageal cancer cells and may provide insights into novel therapeutic strategies for oesophageal cancer.