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Ectopic expression of MECA‐79 as a novel prognostic indicator in gastric cancer
Author(s) -
Okayama Hirokazu,
Kumamoto Kensuke,
Saitou Katsuharu,
Hayase Suguru,
Kofunato Yasuhide,
Sato Yu,
Miyamoto Kotaro,
Nakamura Izumi,
Ohki Shinji,
Koyama Yoshihisa,
Ishii Yoshimasa,
Takenoshita Seiichi
Publication year - 2011
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2011.01895.x
Subject(s) - cancer , immunohistochemistry , metastasis , ectopic expression , gene knockdown , medicine , cancer research , clinical significance , stage (stratigraphy) , survival analysis , oncology , cancer cell , biology , pathology , apoptosis , gene , paleontology , biochemistry
The aim of this study was to clarify the clinical implications of a unique carbohydrate determinant, MECA‐79, in gastric cancer specimens and cells. Immunohistochemical analysis showed that 62 of 225 (27.6%) cases were defined as positive for MECA‐79. MECA‐79 expression was correlated with depth of invasion, venous invasion, TNM stage, and distant metastasis. In survival analyses, patients with MECA‐79 expression had worse prognosis by the log–rank test. Multivariate analysis of the Cox proportional hazard model showed that MECA‐79 expression was an independent factor of a worse cancer‐specific survival. Among 11 gastric cancer cells, MECA‐79 was observed in only MKN7 cells, which also expressed GlcNAc6ST‐2 transcript. A knockdown of GlcNAc6ST‐2 in MKN7 cells showed a markedly reduced expression of MECA‐79, suggesting that GlcNAc‐sulfation of MECA‐79 is mainly synthesized by GlcNAc6ST‐2. Furthermore, real‐time RT‐PCR analysis revealed that GlcNAc6ST‐2 was significantly increased in cancer tissues compared with paired normal mucosa. In conclusion, the expression of MECA‐79 could be a useful marker for the prognosis of gastric cancer. Our results might also provide novel perspectives on the biology of MECA‐79 and GlcNAc6ST‐2 in cancer progression and metastasis. ( Cancer Sci 2011; 102: 1088–1094)

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