Long non-coding RNA-Low Expression in Tumor inhibits the invasion and metastasis of esophageal squamous cell carcinoma by regulating p53 expression.

Autor: PENG-LI WANG, BIN LIU, YANG XIA, CHUN-FENG PAN, TENG MA, YI-JIANG CHEN
Předmět:
Zdroj: Molecular Medicine Reports; 2016, Vol. 13 Issue 4, p3074-3082, 9p
Abstrakt: Long non-coding RNAs (lncRNAs) are involved in governing fundamental biological processes, and, in many lncRNAs, the expression level is altered and likely to have a functional role in tumorigenesis, including apoptosis, migration and invasion. The lncRNA-Low Expression in Tumor (LET), a recently identified lncRNA, was demonstrated to be downregulated in hepatocellular and gallbladder cancer. However, its role in esophageal squamous cell carcinoma (ESCC) requires investigation. The expression level of lncRNA-LET mRNA in primary ESCC and matched healthy tissues (48 cases) was determined by reverse transcription-quantitative polymerase chain reaction. In addition, the effects of lncRNA-LET on cell apoptosis were evaluated by flow cytometric analysis, the regulatory effect of lncRNA-LET on migration was detected using a wound healing assay and cellular invasion was analyzed by Matrigel-coated transwell assay. Furthermore, the effect of lncRNA-LET on cell proliferation was investigated by 5-ethynyl-2'-deoxyuridine cell proliferation assay and protein levels of lncRNA-LET targets were analyzed by western blotting. lncRNA-LET expression was decreased in primary ESCC tissues when compared with paired healthy tissues, and was identified to be associated with the clinical features. Overexpression of lncRNA-LET was observed to inhibit the migration and invasion of ESCC cells, and modulate p53 expression levels in human ESCC cell lines in vitro. These results establish that lncRNA-LET is significant in the regulation of tumor progression and metastasis, and serves as a tumor suppressor in, and therefore has therapeutic potential for, the treatment of human ESCC. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index