Apigenin inhibits the GLUT-1 glucose transporter and the phosphoinositide 3-kinase/akt pathway in human pancreatic cancer cells

Laleh G. Melstrom, Mohammad R. Salabat, Xian Zhong Ding, Benjamin M. Milam, Matthew Strouch, Jill C. Pelling, David J. Bentrem

Research output: Contribution to journalArticle

80 Scopus citations


OBJECTIVES:: The antiproliferative mechanisms of flavonoid drugs inpancreatic cancer cells remain unclear. In this study, we evaluated the effects of the flavonoid apigenin on glucose uptake, on the expression of the glucose transporter 1 (GLUT-1), and on the phosphoinositide 3-kinase (PI3K)/Akt pathway in human pancreatic cancer cells. METHODS:: Human pancreatic cancer cells were treated with apigenin and then underwent glucose uptake assays. Real-time reverse transcription-polymerase chain reaction and Western blot analysis were conducted to evaluate GLUT-1 and pAkt expression in CD18 and S2-013 human pancreatic cancer cells after treatment with apigenin or PI3K inhibitors (LY294002 and wortmannin). RESULTS:: Apigenin (0-100 μM) significantly inhibited, in a dose-dependent fashion, glucose uptake in CD18 and S2-013 human pancreatic cancer cell lines. Apigenin inhibited both GLUT-1 mRNA and protein expression in a concentration- and time-dependent fashion. The PI3K inhibitors, like apigenin, downregulated both GLUT-1 mRNA and protein expression. CONCLUSIONS:: Our results demonstrate that the flavonoid apigenin decreases glucose uptake and downregulates the GLUT-1 glucose transporter in human pancreatic cancer cells. In addition, the inhibitory effects of apigenin and the PI3K inhibitors on GLUT-1 are similar, indicating that the PI3K/Akt pathway is involved in mediating apigenin's effects on downstream targets such as GLUT-1.

Original languageEnglish (US)
Pages (from-to)426-431
Number of pages6
Issue number4
StatePublished - Nov 1 2008



  • Apigenin
  • Flavonoid
  • GLUT-1
  • PI3K/Akt
  • Pancreatic cancer

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Hepatology
  • Endocrinology

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