These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Metformin Promotes 2-Deoxy-2-[18F]Fluoro-D-Glucose Uptake in Hepatocellular Carcinoma Cells Through FoxO1-Mediated Downregulation of Glucose-6-Phosphatase.
    Author: Wang Z, Kang F, Gao Y, Liu Y, Xu X, Ma X, Ma W, Yang W, Wang J.
    Journal: Mol Imaging Biol; 2018 Jun; 20(3):388-397. PubMed ID: 29256045.
    Abstract:
    PURPOSE: The early diagnosis of primary hepatocellular carcinoma (HCC) has the potential to lead to significant improvements for the treatment and survival rates of cancer patients. 2-Deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) is often used as a tracer for positive emission tomography (PET) and X-ray computed tomography (CT) imaging of cancer cells; however, [18F]FDG PET/CT cannot currently be used as an early diagnostic technique for HCC. This is because these cancer cells express high levels of glucose-6-phosphatase (G6Pase) that is responsible for poor cellular retention of [18F]FDG. Here, we sought to investigate the feasibility of metformin treatment to promote [18F]FDG uptake in HCC and the mechanism involved. PROCEDURES: Human SMMC-7721 HCC cells were treated with metformin (up to 10 mM) or FoxO1 siRNA. The transcriptional and expression levels of FoxO1 and G6Pase were determined by quantitative RT-PCR and Western blotting, respectively. The feasibility of using metformin to promote [18F]FDG uptake was investigated by both in vitro cell uptake analysis and in vivo microPET/CT imaging. Stable doxycycline-inducible cell lines with FoxO1-overexpression (FoxO1-OE) and FoxO1-knockdown (FoxO1-KD) were constructed to evaluate the impact of FoxO1 on G6Pase expression in vitro and [18F]FDG uptake in vivo. RESULTS: Treatment of HCC cells with metformin (Met) leads to a dose-dependent reduction in the expression levels of FoxO1 at the protein level, but not at the mRNA level. Met-induced phosphorylation of FoxO1 initiates a reduction in the expression levels of G6Pase mRNA, which results in an overall increase in the uptake of [18F]FDG into HCC cells and tumors. CONCLUSIONS: We propose that treatment of HCC cells with Met may be a useful strategy for improving the efficacy of [18F]FDG as a tracer for PET/CT imaging of HCC tumors in patients.
    [Abstract] [Full Text] [Related] [New Search]