SPOCK1 promotes the proliferation, migration and invasion of glioma cells through PI3K/AKT and Wnt/β-catenin signaling pathways.
Sparc/osteonectin, cwcv and kazal-like domains proteoglycan (testican) 1 (SPOCK1) has been reported to promote the growth and progression of various tumors. In this study, we focus on assessing the effect of SPOCK1 on proliferation, migration and invasion in glioma cells and elucidating its related mechanisms. The results of our present study demonstrated that overexpression of SPOCK1 promoted the proliferation and inhibited apoptosis in glioma cells. Additionally, overexpression of SPOCK1 promoted the migration and invasion potential of glioma cells. Moreover, we demonstrated that PI3K/AKT and Wnt/β-catenin signaling pathways were activated by SPOCK1 over-expression. SPOCK1 silencing has precisely the opposite effect. In conclusion, our study suggests that SPOCK1 promotes proliferation, migration and invasion in glioma cells by activating PI3K/AKT and Wnt/β-catenin pathways, which provides a potential theoretical basis for clinical treatment of glioma.
Department of Hepatopancreatobiliary Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Jinghui
J
Yang
Central Laboratory, Second Hospital, Jilin University, Changchun, Jilin 130041, P.R. China.
Qiwei
Q
Yang
Department of Nephrology, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Jing
J
Yu
Central Laboratory, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130012, P.R. China.
Ximeng
X
Li
Department of Neurology, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Shan
S
Yu
Department of Hepatopancreatobiliary Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Xuewen
X
Zhang
D017209:Apoptosis / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D005910:Glioma / Q000473:pathology*; D006801:Humans; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D009361:Neoplasm Invasiveness / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D011509:Proteoglycans / Q000235:genetics*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D060449:Wnt Signaling Pathway / Q000235:genetics*; D051028:bcl-2-Associated X Protein / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism
D018809:Proliferating Cell Nuclear Antigen; D011509:Proteoglycans; D019253:Proto-Oncogene Proteins c-bcl-2; D034741:RNA, Small Interfering; C504369:SPOCK1 protein, human; D051028:bcl-2-Associated X Protein; D051176:beta Catenin; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9