leads to G1 arrest by p53 pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is the fourth most common cause of cancer death in China. Long noncoding RNAs have emerged as critical regulators in cancer. Long intergenic noncoding ， a kind of Long noncoding RNAs， have been discussed dysregulated in several cancers， but its role in ESCC remains unknown. This study investigated the role of in ESCC. The expression level and its association with esophageal cancer was determined in 64 tumor tissues of esophageal squamous cell carcinoma patients and cells using quantitative real-time reverse transcription PCR. Fluorescence in situ hybridization of single-RNA molecular probes was used to determine subcellular localization of . CCK8 and EdU assays were used for proliferation assay， flow cytometry was performed for apoptosis and cell-cycle distribution， and 24-well Mill cell chamber was made for measuring the abilities of migration and invasion after transfected with lentivirus-expressing in EC109 cells. Then， quantitative real-time reverse transcription PCR and Western blot detected the expression of p21. Further， UC2288， an inhibitor of p21， was used to decrease the level of p21， and flow cytometry was used to detect cell cycle. Finally， screening for differential pathways from microarray analysis and expression of p53 and cyclin D were detected by Western blot. expression level was remarkably lower in tumor tissues versus nontumor tissues and lower in EC109 cells versus Het-1A cells. Statistical analysis found that might enhance the risk of ESCC. We observed that was expressed both in the nucleus and cytoplasm， and a larger proportion of was observed in the cytoplasm. The results demonstrated that upregulating the expression of could inhibit cell proliferation， migration， invasion， and the transition of cell cycle from G1 and promoted apoptosis of EC109. Then， we found that promotes the expression of p21. Decreasing the level of p21 revealed that cell-cycle arrest was restored. Pathway analysis found p53 pathway was downregulated， and upregulation of inhibited the expression of cyclin D. Our study suggests that plays as a tumor inhibitor in ESCC development and might induce G1 arrest through p53 signal pathway.