LINC01232 Facilitates the Proliferation of Esophageal Squamous Cell Carcinoma by Sponging miR-708-5p to Upregulate Upstream Stimulatory Factor 1

Author:

Chen Jian1,Meng Jingjing2,Zhao Yongsheng1,Zhang Lin1,Jia Ke1

Affiliation:

1. Department of Thoracic Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China

2. Department of Hepatological Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, China

Abstract

LncRNAs are vital regulators in human diseases. LINC01232 is found to be upregulated in esophageal squamous cell carcinoma (ESCC). This study aims to uncover the biological functions of LINC01232 in the development of ESCC and the underlying mechanism. Expression pattern of LINC01232 and its influence on the prognosis in ESCC were determined by analyzing the dataset downloaded from TCGA. LINC01232 levels in ESCC tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Regulatory effects of LINC01232 on proliferative and apoptotic abilities in ESCC were examined by Cell Counting Kit (CCK-8) assay, colony formation assay and flow cytometry, respectively. The interaction in the LINC01232/miR-708-5p/USF1 axis was tested by dual-luciferase reporter assay. By analyzing ESCC profiling downloaded from TCGA, LINC01232 was found to be upregulated in ESCC tissues, while its level was unrelated to overall survival and disease-free survival in ESCC patients. LINC01232 was further confirmed to be highly expressed in ESCC tissues and cell lines we collected. Knockdown of LINC01232 inhibited proliferative ability and induced apoptosis in ESCC cells. LINC01232 competed with USF1 to bind miR-708-5p, and thereafter regulated the development of ESCC. LINC01232/miR-708-5p/USF1 axis is responsible for facilitating the proliferative ability in ESCC, thereby aggravating the malignant development of ESCC.

Publisher

American Scientific Publishers

Subject

General Materials Science

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