Keita Katsurahara1, Atsushi Shiozaki2, Toshiyuki Kosuga1, Michihiro Kudou1, Katsutoshi Shoda1, Tomohiro Arita1, Hirotaka Konishi1, Shuhei Komatsu1, Takeshi Kubota1, Hitoshi Fujiwara1, Kazuma Okamoto1, Mitsuo Kishimoto3, Eiichi Konishi3, Yoshinori Marunaka4,5,6,7, Eigo Otsuji1. 1. Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan. 2. Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan. shiozaki@koto.kpu-m.ac.jp. 3. Department of Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan. 4. Department of Molecular Cell Physiology, Kyoto Prefectural University of Medicine, Kyoto, Japan. 5. Research Institute for Clinical Physiology, Kyoto Industrial Health Association, Kyoto, Japan. 6. Research Center for Drug Discovery and Pharmaceutical Development Science, Research Organization of Science and Technology, Ritsumeikan University, Kusatsu, Japan. 7. International Research Center for Food Nutrition and Safety, College of Food and Biological Engineering, Jiangsu University, Zhenjiang, China.
Abstract
BACKGROUND: Few studies have reported the function and activation mechanism of ANO9 in esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the role of ANO9 in the regulation of tumor progression. METHODS: Knockdown experiments with human ESCC cell lines were performed using ANO9 siRNA, and the effects on cell proliferation, the cell cycle, apoptosis, and cellular movement were analyzed. Immunohistochemistry (IHC) analysis was performed on 57 primary tumor samples obtained from ESCC patients. RESULTS: In an in vitro study, depletion of ANO9 reduced cell proliferation, invasion, and migration in KYSE150 and KYSE 790 cells. In the cell cycle analysis, depletion of ANO9 increased the number of cells in G0/G1 arrest. In addition, the knockdown of ANO9 increased apoptosis. The results of the microarray analysis indicated that various centrosome-related genes such as CEP120, CNTRL, and SPAST were up- or downregulated in ANO9-depleted KYSE150 cells. The IHC results showed that high expression of ANO9 was associated with poor prognosis. CONCLUSIONS: The results of the current study suggest that ANO9 regulates the cell cycle via centrosome-related genes in ESCC.
BACKGROUND: Few studies have reported the function and activation mechanism of ANO9 in esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the role of ANO9 in the regulation of tumor progression. METHODS: Knockdown experiments with humanESCC cell lines were performed using ANO9 siRNA, and the effects on cell proliferation, the cell cycle, apoptosis, and cellular movement were analyzed. Immunohistochemistry (IHC) analysis was performed on 57 primary tumor samples obtained from ESCCpatients. RESULTS: In an in vitro study, depletion of ANO9 reduced cell proliferation, invasion, and migration in KYSE150 and KYSE 790 cells. In the cell cycle analysis, depletion of ANO9 increased the number of cells in G0/G1 arrest. In addition, the knockdown of ANO9 increased apoptosis. The results of the microarray analysis indicated that various centrosome-related genes such as CEP120, CNTRL, and SPAST were up- or downregulated in ANO9-depleted KYSE150 cells. The IHC results showed that high expression of ANO9 was associated with poor prognosis. CONCLUSIONS: The results of the current study suggest that ANO9 regulates the cell cycle via centrosome-related genes in ESCC.