title: Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro.
abstract: Osteosarcoma (OS) is the most common malignant tumor of bone. It has recently been demonstrated that galectin-3, a multifunctional β-galactoside-binding, is significantly upregulated in OS tissues, and is correlated with its progression and metastasis. However, the detailed role of galectin‑3 in the regulation of cellular biological processes in OS cells has remained to be elucidated. The present study reported that the mRNA and protein levels of galectin‑3 were significantly increased in OS tissues compared to those in their matched normal adjacent tissues. Furthermore, galectin‑3 was upregulated in three OS cell lines, Saos‑2, MG63 and U2OS, when compared with that in the human osteoblast cell line hFOB1.19. Knockdown of galectin‑3 by galectin‑3‑specific small interfering RNA markedly inhibited OS‑cell proliferation and induced cell apoptosis. Furthermore, silencing of galectin‑3 expression significantly inhibited OS cell migration and invasion, accompanied with a marked decrease in the protein expression of matrix metalloproteinase 2 and ‑9. Mechanistic investigation suggested that the mitogen‑activated protein kinase kinase/extracellular signal‑regulated protein kinase signaling pathway may be involved in the galectin‑3‑mediated OS cell invasion. In conclusion, the present study was the first to report that silencing of galectin‑3 inhibited the malignant phenotypes of osteosarcoma in vitro. Therefore, galectin-3 may serve as a potential therapeutic target for OS.
authors.affiliation: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
authors.forename: Pengfei
authors.initials: P
authors.lastname: Lei
authors.affiliation: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
authors.forename: Hongbo
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
authors.forename: Yihe
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Department of Orthopedics, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.
authors.forename: Zhan
authors.initials: Z
authors.lastname: Liao
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D001798:Blood Proteins; D001859:Bone Neoplasms / Q000188:drug therapy; D045744:Cell Line, Tumor / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D037502:Galectin 3 / Q000235:genetics* / Q000378:metabolism; D037161:Galectins; D020868:Gene Silencing; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D012516:Osteosarcoma / Q000473:pathology*; D010641:Phenotype; D034741:RNA, Small Interfering / Q000494:pharmacology*; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D001798:Blood Proteins; D037502:Galectin 3; D037161:Galectins; C428445:LGALS3 protein, human; D034741:RNA, Small Interfering; D020929:Mitogen-Activated Protein Kinase Kinases; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9