Downregulation of KIF23 suppresses glioma proliferation

Satoshi Takahashi, Noemi Fusaki, Shigeki Ohta, Yoshihiro Iwahori, Yukihiko Iizuka, Kohei Inagawa, Yutaka Kawakami, Kazunari Yoshida, Masahiro Toda

研究成果: Article査読

64 被引用数 (Scopus)

抄録

To identify therapeutic molecular targets for glioma, we performed modified serological identification of antigens by recombinant complementary DNA (cDNA) expression cloning using sera from a mouse glioma model. Two clones, kinesin family member 23 (Kif23) and structural maintenance of chromosomes 4 (Smc4), were identified as antigens through immunological reaction with sera from mice harboring synergic GL261 mouse glioma and intratumoral inoculation with a mutant herpes simplex virus. The human Kif23 homolog KIF23 is a nuclear protein that localizes to the interzone of mitotic spindles, acting as a plus-end-directed motor enzyme that moves antiparallel microtubules in vitro. Expression analysis revealed a higher level of KIF23 expression in glioma tissues than in normal brain tissue. The introduction of small interfering RNA (siRNA) targeting KIF23 into two different glioma cell lines, U87MG and SF126, downregulated KIF23 expression, which significantly suppressed glioma cell proliferation in vitro. KIF23 siRNA-treated glioma cells exhibited larger cell bodies with two or more nuclei compared with control cells. In vivo analysis using mouse xenograft showed that KIF23 siRNA/DNA chimeratreated tumors were significantly smaller than tumors treated with control siRNA/DNA chimera. Taken together, our results indicate that downregulation of KIF23 decreases proliferation of glioma cells and that KIF23 may be a novel therapeutic target in malignant glioma.

本文言語English
ページ(範囲)519-529
ページ数11
ジャーナルJournal of Neuro-Oncology
106
3
DOI
出版ステータスPublished - 2012 2月

ASJC Scopus subject areas

  • 腫瘍学
  • 神経学
  • 臨床神経学
  • 癌研究

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