title: Gene silencing of galectin-3 changes the biological behavior of Eca109 human esophageal cancer cells.
abstract: Galectin-3 is a multifunctional β-galactoside‑binding lectin that is involved in multiple biological functions which are upregulated in malignancies, including cell growth, adhesion, proliferation, progression and metastasis, as well as apoptosis. A previous study has confirmed the roles of galecin-3 overexpression in the biological behavior of Eca109 human esophageal cancer (EC) cells. In the present study, small interfering (si)RNA-mediated galectin-3 silencing was performed to analyze the effects of decreased galectin-3 expression on the biological behavior of EC cells. Western blot and quantitative polymerase chain reaction analyses were utilized to confirm galectin-3 knockdown at the protein and mRNA level (P<0.05 vs. siRNA-control and untransfected groups). Cell proliferation was assessed using the Cell Counting Kit-8 assay. At 72 and 96 h after transfection, the proliferation of Eca109 cells in the siRNA-Gal-3 group was decreased compared with that in the siRNA-Control and untransfected groups (P<0.001 and P=0.004, respectively). Furthermore, Transwell assays demonstrated that inhibition of galecin-3 significantly reduced the migration and invasion of Eca109 cells compared with that in the other groups (P<0.05). Finally, apoptosis of Eca109 cells was detected using Annexin V/7-amino‑actinomycin double-staining and flow cytometric analysis. Galectin-3 knockdown significantly enhanced the apoptotic rate of Eca109 cells compared with that in the siRNA-control and untreated groups (P=0.031 and P=0.047, respectively). In conclusion, following successful knockdown of galecin-3 expression in Eca109 cells, the cell proliferation, migration and invasion were reduced, while the apoptosis was enhanced, which indicates that galectin silencing may represent a therapeutic strategy for EC.
authors.affiliation: Department of Radiation Oncology, Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.
authors.forename: Lili
authors.initials: L
authors.lastname: Qiao
authors.affiliation: Department of Radiation Oncology, Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.
authors.forename: Ning
authors.initials: N
authors.lastname: Liang
authors.affiliation: Department of Radiation Oncology, Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.
authors.forename: Jian
authors.initials: J
authors.lastname: Xie
authors.affiliation: Graduate School, Weifang Medical College, Weifang, Shandong 261053, P.R. China.
authors.forename: Hui
authors.initials: H
authors.lastname: Luo
authors.affiliation: Graduate School, Weifang Medical College, Weifang, Shandong 261053, P.R. China.
authors.forename: Jingxin
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Radiation Oncology, Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.
authors.forename: Guodong
authors.initials: G
authors.lastname: Deng
authors.affiliation: Graduate School, Taishan Medical College, Taian, Shandong 271021, P.R. China.
authors.forename: Yupeng
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Radiation Oncology, Qianfoshan Hospital, Shandong University, Jinan, Shandong 250014, P.R. China.
authors.forename: Jiandong
authors.initials: J
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D004938:Esophageal Neoplasms / Q000235:genetics / Q000473:pathology*; D037502:Galectin 3 / Q000235:genetics / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D020868:Gene Silencing; D006801:Humans; D009361:Neoplasm Invasiveness; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D015203:Reproducibility of Results
chemical_list: D037502:Galectin 3; D012333:RNA, Messenger; D034741:RNA, Small Interfering