Abstract
Expression Characteristics and Biological Functions of MARCKSL1 Targeted and Regulated by microRNA-34a in Esophageal Squamous Cell Carcinoma
Department of Radiation Oncology, 1Department of Oncology, 2Department of Ultrasound, Lishui Branch, Southeast University Affiliated Zhongda Hospital and Lishui District People's Hospital, Nanjing, Jiangsu Province 211200, 3Department of Radiation Oncology, Jiangsu Cancer Hospital, Nanjing, Jiangsu Province 210009, Ch ina
Correspondence Address:
Jiangang Liu, Department of Radiation Oncology, Lishui Branch, Southeast University Affiliated Zhongda Hospital and Lishui District People's Hospital, Nanjing, Jiangsu Province 211200, China, E-mail: 13685104715@163.com
The main aim of this study was to investigate the biological characteristics of myristoylated alanine-rich C-kinase substrate analog-1 expression in esophageal squamous cell carcinoma tissues. Tumor tissues and associated paracancerous tissues were obtained from 74 individuals with esophageal squamous cell carcinoma hospitalized in Nanjing Lishui District People's Hospital between January 2016 and July 2019. According to immunohistochemically findings, the expression level of myristoylated alanine-rich C-kinase substrate analog-1 was comparable to that of patients, and its H-score in esophageal squamous cell carcinoma tissues was substantially greater than that in the equivalent paracancerous tissues (120.10±1.935 vs. 35.65±2.012, t=30.25, p<0.01). The tumor, node and metastasis staging was closely related (χ2=7.835, p<0.01). The expression of myristoylated alanine-rich C-kinase substrate analog-1 emerged as a significant independent risk indicator for overall survival in esophageal squamous cell carcinoma patients, as determined by Cox regression univariate and multivariate analysis (p=0.007; p=0.017). Cytological tests revealed that myristoylated alanine-rich C-kinase substrate analog-1 knockdown may substantially decrease esophageal squamous cell carcinoma cell proliferation, invasion, and migration. According to Western blotting experiments, the epithelial-mesenchymal transition process in esophageal squamous cell carcinoma cells might be inhibited by suppressing myristoylated alanine-rich C-kinase substrate analog-1. The outcomes of the bioinformatics study revealed that post-transcriptional regulation was connected to the dysregulated expression of myristoylated alanine-rich C-kinase substrate analog-1 in the tissues of esophageal cancer. Upstream mechanism experiments confirmed that microRNA-34a, the "suppressor" of esophageal cancer, can target myristoylated alanine-rich C-kinase substrate analog-1 and inhibit its expression at the post-transcriptional level. The current study demonstrated that myristoylated alanine-rich C-kinase substrate analog-1 may function as an "oncogene" in esophageal squamous cell carcinoma. The outcome of this investigation suggests that myristoylated alanine-rich C-kinase substrate analog-1 could become a potentially new biomarker in diagnosing esophageal squamous cell carcinoma and a new target for tumor therapy.
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