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Dysregulated expression of HOX and ParaHOX genes in human esophageal squamous cell carcinoma

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Title: Dysregulated expression of HOX and ParaHOX genes in human esophageal squamous cell carcinoma
Authors: Takahashi, Osamu Browse this author
Hamada, Jun-ichi Browse this author
Abe, Motoki Browse this author
Hata, Shinya Browse this author
Asano, Toshimichi Browse this author
Takahashi, Yoko Browse this author
Tada, Mitsuhiro Browse this author
Miyamoto, Masaki Browse this author
Kondo, Satoshi Browse this author →KAKEN DB
Moriuchi, Tetsuya Browse this author
Keywords: homeobox gene
HOX
real-time RT-PCR
esophageal cancer
ParaHOX
Issue Date: Apr-2007
Publisher: Spandidos Publications
Journal Title: Oncology Reports
Volume: 17
Issue: 4
Start Page: 753
End Page: 760
Abstract: Homeobox genes function as master regulators in embryonic morphogenesis. We hypothesized that homeobox genes are essential to maintain tissue- or organ-specificity even in adult body and that the dysregulated expression of homeobox genes results in tumor development and progression. To better understand the roles of homeobox genes in development and progression of esophageal cancer, we analyzed the expression patterns of 39 HOX genes and 4 ParaHOX (CDX1, CDX2, CDX4 and PDX1) genes in esophageal squamous cell carcinoma (ESCC) and normal esophageal mucosa tissues. A total of 48 primary ESCC tissues and 7 normal esophageal mucosa tissues were resected from patients who underwent radical surgery without any preoperative chemotherapy or radiotherapy. The expression of HOX and ParaHOX genes were analyzed by a quantitative real-time RT-PCR method and immunohistochemistry. The expression levels of 24 HOX genes, CDX1, CDX2 and PDX1 were significantly higher in ESCC compared to normal mucosa (p<0.01, Mann-Whitney U test). The Immunohistochemical study revealed that HOXA5 and D9 proteins were more cytoplasmic in ESCC than normal mucosa cells. Our data indicate that the disordered expression of HOX and ParaHOX genes are involved in the development of ESCC or its malignancy.
Type: article
URI: http://hdl.handle.net/2115/42833
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 浜田 淳一

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