Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Hui Chen
Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Shuang Xu
Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Cong‐Rui Liao
Division of Spine Surgery Department of Orthopaedics Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Anran Xu
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Yue Han
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Min‐Hui Yang
Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Li Zhao
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Sha‐Sha Hu
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Lan Wang
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Qing‐Yuan Li
Guangdong Provincial Key Laboratory of Gastroenterology Department of Gastroenterology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Ling‐Ying Zhan
Department of Pathology School of Basic Medical Sciences Southern Medical University Guangzhou Guangdong China
Yan‐Qing Ding
Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Shuang Wang
Department of Pathology Nanfang Hospital Southern Medical University Guangzhou Guangdong China
Abstract Mounting evidence has demonstrated the considerable regulatory effects of long noncoding RNAs (lncRNAs) in the tumorigenesis and progression of various carcinomas. LncRNA Semaphorin 3B (SEMA3B) antisense RNA 1 (SEMA3B‐AS1) has been found to be dysregulated in a few carcinomas recently. However, its potential function and mechanism in colorectal carcinoma (CRC) have not yet been examined. Here we show that SEMA3B‐AS1 acts as a crucial regulator of CRC progression. We found that SEMA3B‐AS1 expression was downregulated in CRC cell lines and tissues. Downregulation of SEMA3B‐AS1 was significantly associated with poor survival in CRC patients. Overexpression of SEMA3B‐AS1 reduced the cell growth and metastasis of CRC in vivo and in vitro. In addition, SEMA3B‐AS1 promoted the expression of its sense‐cognate gene SEMA3B, a member of the Semaphorin family (SEMAs), by recruiting EP300 to induce H3K9 acetylation at the SEMA3B promoter. Furthermore, we proved that SEMA3B‐AS1 suppressed CRC angiogenesis by affecting the vascular endothelial growth factor signaling pathway activation which was regulated by the SEMA3B‐NRP1 axis. Our work unravels a novel mechanism of SEMA3B‐AS1 in the inhibition of CRC malignant progression and highlights its probability as a new promising diagnostic marker and therapeutic target for CRC interventions.