Gene profiling of MAPK pathway in human osteosarcoma.
- Author:
Guo-dong LI
1
;
Zheng-dong CAI
;
Yin-quan ZHANG
;
Hai-yang GONG
;
Hao TANG
;
Qiu-lin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Aged; Bone Neoplasms; genetics; metabolism; pathology; Cell Line, Tumor; Child; Female; Gene Expression Profiling; Humans; JNK Mitogen-Activated Protein Kinases; metabolism; Male; Middle Aged; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Mitogen-Activated Protein Kinases; metabolism; Oligonucleotide Array Sequence Analysis; Osteoblastoma; genetics; metabolism; pathology; Osteosarcoma; genetics; metabolism; pathology; Signal Transduction; Young Adult; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Chinese Journal of Oncology 2009;31(5):340-345
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the functional effects of MAPK pathway in the pathogenesis of human osteosarcoma.
METHODSGene microarray (Human Genome U133A, Affymetrix) was used to screen the differential expression of genes involved in MAPK pathway between osteosarcoma cell lines and 3 osteoblastic cell lines. KEGG metabolic pathway analysis was performed among significantly increased or decreased genes using the MATLAB software. Immunohistochemical technique was used to detect the expressions of ERK1/2, JNK and p38 proteins among 48 osteosarcoma and benign 24 osteoblastic tumor samples.
RESULTSUsing an entrance limit of > or = 2.0, 18 differentially expressed MAPK pathway-related genes were selected (10 up-regulated, 8 down-regulated) to mapped to the MAPK pathway of KEGG which are all important node genes. The positive rates of ERK1/2, JNK and p38 proteins were 83.3% (40/48), 72.9% (35/48) and 85.4% (41/48) in osteosarcomas,and 12.5% (3/24), 8.3% (2/24) and 16.7% (4/24) in the control group, respectively. The positive rates and expression intensities were statistically different between the 2 groups (P<0.01).
CONCLUSIONMAPK pathway plays an important role in the pathogenesis of osteosarcoma. ERK, JNK and p38 form an intercoordinating network and regulate the cell proliferation, differentiation, apoptosis, invasion and migration in osteosarcoma.