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RGS22, a novel cancer/testis antigen, inhibits epithelial cell invasion and metastasis

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Abstract

RGS22 is a novel testis specific gene. It is located within chromosome 8q22.2, which shows high relevance with tumor chromosomal aberrations. We investigated the potential role of RGS22 in human tumorigenesis. We examined the level of RGS22 expression by tumor tissue arrays, immunohistochemistry and by analyzing the expression levels of four human esophageal cancer cell lines with different metastatic potential using western blot. In addition, we examined the role of RGS22 over-expression in the processes of invasion and metastasis using a highly metastatic cancer cell line. We show that RGS22 are expressed in many tumor types, but specific to cancers with epithelial origin and associated with cancer metastasis. In addition, we identified the association of RGS22 to tumor invasion in cancer cell lines. Over-expression of RGS22 in a highly metastatic esophageal cancer cell line causes decrease in cell migration and reduction in the invasive potential of the cells. RGS22 is over-expressed in low metastatic epithelial cancers and involved in the processes of cell migration and invasion in esophageal cancer cell lines. Therefore, RGS22 may be an important tumor suppressor gene in tumorigenesis, a potential new diagnostic and prognostic biomarker for metastasis and may translate to therapeutic opportunities for the preventive treatment of epithelial cancer metastasis.

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Acknowledgments

This study was supported by 973 Program No. 2006CB504002 and NSFC grants No. 30630030, No. 81000272. We are grateful to Dr. Yutaka Shimada for his permission of KYSE 150, 450, 510 cell lines and Dr. Mingrong Wang for his provision of EC9706 cell line. We’d like also to thank our colleagues for their helpful assistance and advice.

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Correspondence to Zuomin Zhou.

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Yanqiu Hu and Jun Xing are co-first authorship.

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Hu, Y., Xing, J., Wang, L. et al. RGS22, a novel cancer/testis antigen, inhibits epithelial cell invasion and metastasis. Clin Exp Metastasis 28, 541–549 (2011). https://doi.org/10.1007/s10585-011-9390-z

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  • DOI: https://doi.org/10.1007/s10585-011-9390-z

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