PURPOSE

Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 () in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.

METHODS

ESCC tissue samples and paired normal adjacent tissues were collected to quantify expression by reverse-transcription quantitative PCR. The effects of on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.

RESULTS

was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the high-expression group than in the low-expression group. An knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the knockdown.

CONCLUSION

Thus, enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383-SP1 axis, which may represent a novel target for ESCC therapy.