Actin-binding protein Anillin promotes the progression of gastric cancer in vitro and in mice

• Main Authors: Gao, Z. (Author), Jia, H. (Author), Li, B. (Author), Yu, F. (Author)
• Format: Article
• Language: English
• Published: John Wiley and Sons Inc 2021
• Subjects: actin binding protein; adult; anillin; anillin (ANLN); animal; animal experiment; animal model; animal tissue; Animals; ANLN protein, human; Article; bioinformatics; cancer growth; cancer tissue; cell invasion; Cell Line, Tumor; cell migration; cell motion; Cell Movement; cell proliferation; Cell Proliferation; clinical feature; colony formation; controlled study; drug screening; female; Female; gastric cancer (GC); gastric cancer cell line; genetics; human; human cell; human tissue; Humans; immunohistochemistry; in vitro study; in vivo study; invasion; male; Male; metabolism; Mice, Nude; Microfilament Proteins; middle aged; Middle Aged; migration; mouse; nonhuman; nude mouse; pathology; proliferation; protein expression level; stomach cancer; Stomach Neoplasms; stomach tumor; transwell assay; tumor cell line; tumor xenograft; unclassified drug; wound closure; Xenograft Model Antitumor Assays
• Online Access: View Fulltext in Publisher

 Background: To detect the expression levels of actin-binding protein anillin (ANLN) in human gastric cancer (GC) tissues and explore the possible involvement of ANLN in GC cell proliferation, migration, and invasion. Methods: The bioinformation analysis was performed in TCGA database to explore the expression of ANLN in human GC tissues and the difference of ANLN expression between multiple types of cancers. IHC assays and clinical pathological analysis were performed to confirm ANLN expression and its correlation with clinical features of GC patients. Colony formation, CCK-8, wound closure, and transwell assays were performed to detect its effects on GC cell proliferation, migration, and invasion in vitro. Tumor growth was also measured using a xenograft animal model. Results: We found the high expression of ANLN in human GC tissues based on the results from TCGA database and IHC staining. We further noticed ANLN depletion resulted in the inhibition of GC cell proliferation, migration, and invasion. Our data further confirmed that ANLN contributed to tumor growth of GC cells in vivo. Conclusions: We confirmed the involvement of ANLN in GC progression and thought ANLN could serve as a promising therapeutic target for GC. © 2020 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals LLC