Upregulation of miR-494 Inhibits Cell Growth and Invasion and Induces Cell Apoptosis by Targeting Cleft Lip and Palate Transmembrane 1-Like in Esophageal Squamous Cell Carcinoma

• Published in: Digestive diseases and sciences Vol. 60; no. 5; pp. 1247 - 1255
• Main Authors: Zhang, Ren, Chen, Xiaonan, Zhang, Shengjie, Zhang, Xueyan, Li, Tong, Liu, Zhicai, Wang, Jinwu, Zang, Wenqiao, Wang, Yuanyuan, Du, Yuwen, Zhao, Guoqiang
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.05.2015; Springer; Springer Nature B.V
• Subjects: 3' Untranslated Regions; Analysis; Apoptosis; Binding Sites; Biochemistry; Carcinoma, Squamous Cell - genetics; Carcinoma, Squamous Cell - metabolism; Carcinoma, Squamous Cell - pathology; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cleft lip; Esophageal cancer; Esophageal Neoplasms - genetics; Esophageal Neoplasms - metabolism; Esophageal Neoplasms - pathology; Esophageal Squamous Cell Carcinoma; Female; Gastroenterology; Gene Expression Regulation, Neoplastic; Genes; Growth; Hepatology; Humans; Lymphatic Metastasis; Male; Medicine; Medicine & Public Health; Membrane Proteins - genetics; Membrane Proteins - metabolism; MicroRNA; MicroRNAs - genetics; MicroRNAs - metabolism; Middle Aged; Neoplasm Invasiveness; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; Oncology; Original Article; RNA, Messenger - metabolism; Signal Transduction; Squamous cell carcinoma; Time Factors; Transfection; Transplant Surgery; Esophageal squamous cell carcinoma; CLPTM1L; Proliferation; miR-494; Invasion; Apoptosis
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/s10620-014-3433-7

Background Potential target genes of microRNA (miR)-494 have been reported in many types of cancers. However, the role of miR-494 in esophageal squamous cell carcinoma (ESCC) remains unknown. Aim This study focused on the expression and biological function of miR-494 in ESCC. Methods Using bioinformatics analyses, we found that cleft lip and palate transmembrane 1-like (CLPTM1L) was a potential target of miR-494. We performed quantitative real-time (qRT) PCR assays in 37 ESCC tumor tissues to determine the expression of miR-494 and CLPTM1L mRNA, and we analyzed the correlation between both of these factors and clinical characteristics. The cell counting kit-8 and colony formation assays were used to evaluate the effects of miR-494 expression on the proliferation of ESCC cells. The transwell migration assay and flow cytometric apoptosis assay were performed to study the influence of miR-494 on the invasion and apoptosis of ESCC cells. Western blotting, luciferase assays, and CLPTM1L knockdown experiments were used to determine whether CLPTM1L was a target of miR-494. Results The qRT-PCR assays showed significant downregulation of miR-494 ( P  < 0.05) and upregulation of CLPTM1L mRNA ( P  < 0.05), both of which were significantly associated with lymph node metastases ( P  < 0.05). High expression of miR-494 inhibited cell proliferation and invasion and promoted cell apoptosis ( P  < 0.05). The results also showed that CLPTM1L was a target of miR-494. Conclusion These results show that the expression of miR-494, which can regulate cell growth, invasion and apoptosis of ESCC cells by targeting CLPTM1L, is downregulated in ESCC tumor tissues. The miR-494–CLPTM1L pathway could be further exploited to develop a new approach to treat ESCC.