The effect of SYT-SSX and extracellular signal-regulated kinase (ERK) on cell proliferation in Synovial sarcoma

Wenjuan Cai, Yan Sun, Wei Wang, Chunrong Han, Mamoru Oouchida, Wenbin Xia, Xiulan Zhao, Baocun Sun

Research output: Contribution to journalArticle

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Abstract

The character of Synovial sarcoma is the chromosomal translocation t(X; 18)(p11.2;q11.2), which results in the fusion of the SYT gene with a SSX gene. There is little study that could fully elucidate the mechanism of pathogenesis of this fusion transcript. This study is designed to gain more insight into the function of this fusion gene. We evaluated the whole genome expression in SYO-1 cells inhibited as a result of specific small interfering RNA for SYT-SSX. Cell proliferation and apoptosis were analyzed by flow cytometer and MTT. The proteins correlated with proliferation were also detected using western blot. TUNEL and Immunohistochemical stain assessment were also carried out on TMA of SS tissues. The mRNA level reduced over 90% caused by SYT-SSX specific siRNA. Five pathways were employed, that ERK1/2 pathway was differential significantly (p= 0.043218). Meanwhile, down-regulation of SYT-SSX fusion gene expression would inhibit the proliferation of SS cell and the survival rate decreased (34.1%), while apoptotic rate increased (10.92%). After transfected with SYT-SSX-specific siRNA it caused a block in G1/G0 phase (31.99%) of SYO-1 cells compared with control cells. The protein level of ERK1/2, p-ERK, and cyclin D1 altered in same trend with expression of SYT-SSX. In TMA stain assessment, SYT-SSX positive group with high ki-67 LI expressed more cyclin D1 and CDK4 than the SYT-SSX negative group. High ki-67 LI was detected in cases with p-ERK expression. Meanwhile, cyclin D1 and CDK4 were shown to be more expressed in tumor cells with p-ERK expression. Our results suggest that the fusion gene SYT-SSX should be considered to play important role on SS cell growth via ERK pathway. This study may be valuable for understanding the pathogenic role and molecular mechanism of the fusion gene SYT-SSX in synovial sarcoma through the proposed genome-wide approach. Furthermore, the research would open up the possibility of using SYT-SSX and ERK as a therapeutic target.

Original languageEnglish
Pages (from-to)357-367
Number of pages11
JournalPathology and Oncology Research
Volume17
Issue number2
DOIs
Publication statusPublished - Jun 2011

Fingerprint

Synovial Sarcoma
Extracellular Signal-Regulated MAP Kinases
Gene Fusion
Cell Proliferation
Cyclin D1
Small Interfering RNA
Coloring Agents
Genome
Cell Cycle Resting Phase
Genetic Translocation
MAP Kinase Signaling System
Mitogen-Activated Protein Kinase 1
In Situ Nick-End Labeling
G1 Phase
Cell Survival
Proteins
Down-Regulation
Western Blotting
Apoptosis
Gene Expression

Keywords

  • Cell proliferation
  • Fusion gene
  • Synovial sarcoma

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Pathology and Forensic Medicine

Cite this

The effect of SYT-SSX and extracellular signal-regulated kinase (ERK) on cell proliferation in Synovial sarcoma. / Cai, Wenjuan; Sun, Yan; Wang, Wei; Han, Chunrong; Oouchida, Mamoru; Xia, Wenbin; Zhao, Xiulan; Sun, Baocun.

In: Pathology and Oncology Research, Vol. 17, No. 2, 06.2011, p. 357-367.

Research output: Contribution to journalArticle

Cai, Wenjuan ; Sun, Yan ; Wang, Wei ; Han, Chunrong ; Oouchida, Mamoru ; Xia, Wenbin ; Zhao, Xiulan ; Sun, Baocun. / The effect of SYT-SSX and extracellular signal-regulated kinase (ERK) on cell proliferation in Synovial sarcoma. In: Pathology and Oncology Research. 2011 ; Vol. 17, No. 2. pp. 357-367.
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AU - Zhao, Xiulan

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