P-LAP/IRAP-induced cell proliferation and glucose uptake in endometrial carcinoma cells via insulin receptor signaling

Kiyosumi Shibata, Hiroaki Kajiyama, Kazuhiko Ino, Akihiro Nawa, Seiji Nomura, Shigehiko Mizutani, Fumitaka Kikkawa

研究成果: ジャーナルへの寄稿学術論文査読

18 被引用数 (Scopus)

抄録

Background: Hyperglycemia or hyperinsulinemia contributes to poorer endometrial cancer survival. It was shown that P-LAP/IRAP translocates to the plasma membrane in response to insulin stimulation. Recently, we demonstrated that P-LAP/IRAP is associated with a poor prognosis in endometrial adenocarcinoma patients. The aim of this study was to examine whether the malignant potential of endometrial cancer enhanced by P-LAP/IRAP is due to increased glucose uptake via the P-LAP/ IRAP-mediated activation of insulin signaling. Methods: We transfected P-LAP/IRAP cDNA into A-MEC cells (endometrial adenocarcinoma cell line), and A-MEC-LAP cells expressed a remarkably high level of GLUT4 proteins. Results: 3H-2-deoxyglucose uptake which responds to insulin in A-MEC-LAP cells was significantly higher than that of A-MEC-pc cells. A-MEC-LAP cells exhibited a significant growth-stimulatory effect compared to A-MEC-pc cells. A-MEC-LAP cells expressed a remarkably high level of p85PI3K protein compared to A-MEC-pc cells, and showed a higher degree of AKT phosphorylation by insulin stimulation. Conclusion: In summary, P-LAP/IRAP was involved in the increasing malignant potential of endometrial cancer mediated by insulin. P-LAP/ IRAP was suggested to be a potential new target of molecular-targeted therapy for endometrial cancer.

本文言語英語
論文番号15
ジャーナルBMC Cancer
7
DOI
出版ステータス出版済み - 2007
外部発表はい

All Science Journal Classification (ASJC) codes

  • 腫瘍学
  • 遺伝学
  • 癌研究

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