OBJECTIVE: This study aimed to investigate the expression levels of miR-133a-3p and collagen type I α 1 (COL1A1) in esophageal squamous cell carcinoma (ESCC) to find out the relationship between miR-133a-3p and COL1A1 and their influence on ESCC propagation, migration, invasion, and apoptosis. METHODS: The messenger RNA expression levels of miR-133a-3p and COL1A1 in ESCC were detected by quantitative reverse-transcription polymerase chain reaction. The expression of COL1A1 protein was examined via western blot analysis and immunohistochemistry assay. Cell propagation and apoptosis were, respectively, confirmed by CCK-8 and flow cytometry assay, whereas cell mobility and invasiveness were analyzed by wound healing assay and transwell assay. The targeted relationship between miR-133a-3p and COL1A1 was validated by the dual luciferase reporter assay. The tumor xenograft model was constructed to further verify the impact of miR-133a-3p on esophageal squamous tumor growth and COL1A1 expression in vivo. RESULTS: miR-133a-3p was found low-expressed whereas COL1A1 was highly expressed in esophageal squamous cancer tissue and cells. The expression of miR-133a-3p was negatively correlated with COL1A1 expression. The dual luciferase reporter gene assay confirmed that miR-133a-3p directly targeted COL1A1 and suppressed its expression. Cell Counting Kit-8 assay, transwell assay, and flow cytometry analysis demonstrated that COL1A1 promoted ESCC propagation and invasion and suppressed cell apoptosis, whereas miR-133a-3p reversed such adverse effects by regulating COL1A1. CONCLUSIONS: miR-133a-3p inhibited the cell propagation, invasion, and migration and facilitated apoptosis in ESCC by targeting COL1A1.
OBJECTIVE: This study aimed to investigate the expression levels of miR-133a-3p and collagen type I α 1 (COL1A1) in esophageal squamous cell carcinoma (ESCC) to find out the relationship between miR-133a-3p and COL1A1 and their influence on ESCC propagation, migration, invasion, and apoptosis. METHODS: The messenger RNA expression levels of miR-133a-3p and COL1A1 in ESCC were detected by quantitative reverse-transcription polymerase chain reaction. The expression of COL1A1 protein was examined via western blot analysis and immunohistochemistry assay. Cell propagation and apoptosis were, respectively, confirmed by CCK-8 and flow cytometry assay, whereas cell mobility and invasiveness were analyzed by wound healing assay and transwell assay. The targeted relationship between miR-133a-3p and COL1A1 was validated by the dual luciferase reporter assay. The tumor xenograft model was constructed to further verify the impact of miR-133a-3p on esophageal squamous tumor growth and COL1A1 expression in vivo. RESULTS: miR-133a-3p was found low-expressed whereas COL1A1 was highly expressed in esophageal squamous cancer tissue and cells. The expression of miR-133a-3p was negatively correlated with COL1A1 expression. The dual luciferase reporter gene assay confirmed that miR-133a-3p directly targeted COL1A1 and suppressed its expression. Cell Counting Kit-8 assay, transwell assay, and flow cytometry analysis demonstrated that COL1A1 promoted ESCC propagation and invasion and suppressed cell apoptosis, whereas miR-133a-3p reversed such adverse effects by regulating COL1A1. CONCLUSIONS: miR-133a-3p inhibited the cell propagation, invasion, and migration and facilitated apoptosis in ESCC by targeting COL1A1.
Authors: Siri H Strand; Linnéa Schmidt; Simone Weiss; Michael Borre; Helle Kristensen; Anne Karin Ildor Rasmussen; Tina Fuglsang Daugaard; Gitte Kristensen; Hein Vincent Stroomberg; Martin Andreas Røder; Klaus Brasso; Peter Mouritzen; Karina Dalsgaard Sørensen Journal: Sci Rep Date: 2020-07-01 Impact factor: 4.379