Apigenin Inhibits Pancreatic Cancer Cell Proliferation via Down-Regulation of the Glut-1 Glucose Transporter Through the Phosphoinositide 3-Kinase (Pi3k)/Akt Signaling Pathway

Golkar, Laleh; Salabat, Mohammad R.; Ding, Xianzhong; Ujiki, Michael; Rao, Shanta S.; McGill, J. J.; Chen, C.; Heiferman, Daniel M.; Pelling, Jill C.; Talamonti, Mark S.; Bentrem, David J.

doi:10.1097/00006676-200611000-00094

Cited by 2 publications

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“…PI3K pathways also affect insulin-induced glucose transport in fatty cells (113,114). Apigenin downregulates the expression of GLUT-1 mRNA and protein in CD18 and S2-013 pancreatic cancer cell lines, and inhibits the PI3K/Akt channel (49,115). It has been found that inhibition of the PI3K/Akt pathway may induce a decrease in GLUT-1 mRNA (112,116).…”

Section: Association Between Glut-1 and Pi3k/aktmentioning

confidence: 99%

Roles of glucose transporter-1 and the phosphatidylinositol 3-kinase/protein kinase B pathway in cancer radioresistance (Review)

Jin

Zhou

Fan

et al. 2014

Molecular Medicine Reports

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The mechanisms underlying cancer radioresistance remain unclear. Several studies have found that increased glucose transporter‑1 (GLUT‑1) expression is associated with radioresistance. Recently, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway was reported to be involved in the control of GLUT‑1 trafficking and activity. Activation of the PI3K/Akt pathway may itself be associated with cancer radioresistance. Thus, increasing attention has been devoted to the effects of modifying the expression of GLUT‑1 and the PI3K/Akt pathway on the increase in the radiosensitivity of cancer cells. This review discusses the importance of the association between elevated expression of GLUT‑1 and activation of the PI3K/Akt pathway in the development of radioresistance in cancer.

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Section: Association Between Glut-1 and Pi3k/aktmentioning

confidence: 99%

Roles of glucose transporter-1 and the phosphatidylinositol 3-kinase/protein kinase B pathway in cancer radioresistance (Review)

Jin

Zhou

Fan

et al. 2014

Molecular Medicine Reports

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Anticancer Mechanism of Apigenin and the Implications of GLUT-1 Expression in Head and Neck Cancers

et al. 2013

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Apigenin, a natural phytoestrogen flavonoid, has potential biological effects, including antioxidative, anti-inﬂammatory and anticancer activities. The mechanisms of anticancer activities of apigenin are unknown. Some studies have found that apigenin inhibits GLUT-1 mRNA and protein expression in cancer cells. Thus, we hypothesized that apigenin exerts similar effects on head and neck cancers through its inhibition of GLUT-1 expression. In this article, we review the anticancer mechanism of apigenin and the implications of GLUT-1 expression in head and neck cancers. In addition, we describe the current state of knowledge about the relationship between apigenin and GLUT-1 expression in head and neck cancers.

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Apigenin Inhibits Pancreatic Cancer Cell Proliferation via Down-Regulation of the Glut-1 Glucose Transporter Through the Phosphoinositide 3-Kinase (Pi3k)/Akt Signaling Pathway

Cited by 2 publications

References 0 publications

Roles of glucose transporter-1 and the phosphatidylinositol 3-kinase/protein kinase B pathway in cancer radioresistance (Review)

Roles of glucose transporter-1 and the phosphatidylinositol 3-kinase/protein kinase B pathway in cancer radioresistance (Review)

Anticancer Mechanism of Apigenin and the Implications of GLUT-1 Expression in Head and Neck Cancers

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