Overexpression of KIF11 in Gastric Cancer with Intestinal Mucin PhenotypeImai T.a, b · Oue N.a · Nishioka M.a · Mukai S.a · Oshima T.c · Sakamoto N.a · Sentani K.a · Matsusaki K.d · Yoshida K.b · Yasui W.a
aDepartment of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, bDepartment of Surgical Oncology, Graduate School of Medicine, Gifu University, Gifu, cDepartment of Surgery, Yokohama City University, Yokohama, and dKanamecho Hospital, Tokyo, Japan
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Objective: Gastric cancer (GC) is one of the most common human cancers. A useful method of gastric cancer stem cell (CSC) characterization is spheroid colony formation. Previously, we reported that KIF11 expression is >2-fold in spheroid-body-forming GC cells compared with parental cells. Here, we analyzed the expression and distribution of KIF11 in human GC by immunohistochemistry. Methods: Expression of KIF11 in 165 GC cases was determined using immunohistochemistry. For mucin phenotypic expression analysis of GC, immunostaining of MUC5AC, MUC6, MUC2 and CD10 was evaluated. RNA interference was used to inhibit KIF11 expression in GC cell lines. Results: In total, 119 of 165 GC cases (72%) were positive for KIF11. Expression of KIF11 was not associated with any clinicopathologic characteristics; however, it was observed frequently in GC exhibiting an intestinal phenotype. Both the number and size of spheres formed by MKN-74 cells were significantly reduced following transfection of KIF11-targeting siRNA compared with negative-control siRNA. Furthermore, levels of phosphorylated Erk1/2 were lower in KIF11 siRNA-transfected cells than with negative-control siRNA-transfected cells. Conclusion: These results indicate that KIF11 is involved in intestinal mucin phenotype GC.
© 2016 S. Karger AG, Basel
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