OBJECTIVE: Long non-coding RNAs (lncRNAs) have emerged as pivotal participants of various tumors. This manuscript focuses on the function of lncRNA linc01433 (linc01433) in esophageal squamous cell carcinoma (ESCC) development. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect expressions of linc01433 and microRNA-1301 (miR-1301) in ESCC tissues and cells. Cell counting kit-8 (CCK-8) and colony formation assays were used to verify proliferative ability changes in ESCC influenced by linc01433 and miR-1303. Wound healing and transwell assays were chosen to determine migratory ability in ESCC cells. RESULTS: Linc01433 was abnormally up-regulated in ESCC tissues and cells. High level of linc01433 was positively correlated with tumor size and lymph node metastasis in ESCC patients. Up-regulation of linc01433 promoted cell proliferation and migration. MiR-1301 was a potential target of linc01433, and its level was negatively regulated by linc01433. MiR-1301 was responsible for linc01433-regulated proliferation and migration of ESCC. CONCLUSIONS: Linc01433 participated in ESCC progression by regulating miR-1301 and it could function as a novel biomarker in ESCC diagnosis and treatment.
OBJECTIVE: Long non-coding RNAs (lncRNAs) have emerged as pivotal participants of various tumors. This manuscript focuses on the function of lncRNA linc01433 (linc01433) in esophageal squamous cell carcinoma (ESCC) development. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect expressions of linc01433 and microRNA-1301 (miR-1301) in ESCC tissues and cells. Cell counting kit-8 (CCK-8) and colony formation assays were used to verify proliferative ability changes in ESCC influenced by linc01433 and miR-1303. Wound healing and transwell assays were chosen to determine migratory ability in ESCC cells. RESULTS:Linc01433 was abnormally up-regulated in ESCC tissues and cells. High level of linc01433 was positively correlated with tumor size and lymph node metastasis in ESCC patients. Up-regulation of linc01433 promoted cell proliferation and migration. MiR-1301 was a potential target of linc01433, and its level was negatively regulated by linc01433. MiR-1301 was responsible for linc01433-regulated proliferation and migration of ESCC. CONCLUSIONS:Linc01433 participated in ESCC progression by regulating miR-1301 and it could function as a novel biomarker in ESCC diagnosis and treatment.