Apigenin Inhibits the GLUT-1 Glucose Transporter and the Phosphoinositide 3-Kinase/Akt Pathway in Human Pancreatic Cancer Cells

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

doi:10.1097/mpa.0b013e3181735ccb

Cited by 136 publications

(137 citation statements)

References 22 publications

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“…The PI3K/Akt pathway has been shown to promote both GLUT-1 cell-surface trafficking and activity (14,15). The activation and phosphorylation of PI3K/Akt are not only well-recognized regulators of cell growth, survival and angiogenesis, but they also play an important role in promoting glucose metabolism (28).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly to the insulin-responsive glucose transporter GLUT-4, GLUT-1 cell-surface localization is controlled by extrinsic signals. Among the signaling pathways initiated in cell activation, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway has been shown to promote both GLUT-1 cell-surface trafficking and activity (14,15).…”

Section: Introductionmentioning

confidence: 99%

“…PI3K is a heterodimeric enzyme important for growth and proliferation and Akt is a downstream serine-threonine kinase that transmits survival signals from growth factors (15). The PI3K/Akt pathway is frequently overactive in various tumors and triggers a cascade of responses, from cell growth and proliferation to cell survival and motility, which drives tumor progression (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

“…The PI3K/Akt pathway is frequently overactive in various tumors and triggers a cascade of responses, from cell growth and proliferation to cell survival and motility, which drives tumor progression (15)(16)(17). The PI3K/Akt pathway has been shown to be involved in translocating the GLUT-1 glucose transporter from the cytosol to the plasma membrane in endocrine organs such as the pancreas (15).…”

Section: Introductionmentioning

confidence: 99%

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Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

et al. 2012

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Abstract. The purpose of this study was to explore the factors associated with the recurrence of adenoid cystic carcinomas (ACCs). We examined the recurrence values of clinicopathological variables and GLUT-1, p-Akt and PI3K expression in 42 patients with ACC. Of the 42 patients, 17 developed recurrence following initial surgery. The positive rates of GLUT-1, PI3K and p-Akt protein expression in ACC were 38.1, 38.1 and 50.0%, respectively. The expression of GLUT-1, p-Akt or PI3K protein in ACC was higher than that in inflammatory lesions or benign tumors. Our study demonstrated that T stage, a positive resection margin, perineural invasion, surgery without postoperative radiotherapy and the expression of GLUT-1, PI3K and p-Akt were factors predictive of recurrence by univariate analyses. In multivariate analyses, perineural invasion, a positive resection margin and p-Akt were significant predictors of recurrence. Initial surgery is very significant in the recurrence of ACC. Overexpression of GLUT-1, PI3K and p-Akt may also play a role in its development and recurrence.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

et al. 2012

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“…Research has shown that in human tongue squamous carcinoma (SCC-9) and human esophageal cancer (both KYSE-510 and OE33), after exposure to apigenin, the level of cells in the G1 phase (when the cells grow in size and mRNA and high amounts of protein are synthesized) decreased, while the level of cells in the third stage of interphase (the G2 phase) increased. 16 This is associated with the down-regulation of protein cyclin B1 and the up-regulation of p53-inducible gene 3 and protein p21-WAF1. P21-WAF1 is responsible for G1 phase arrest and the G2/M checkpoint, and apigenin in concentration levels higher than 30 μM increases the transcription of this protein.…”

Section: Modification Of the Cell Cyclementioning

confidence: 99%

Insights into novel anticancer applications for apigenin

Kowalczyk¹,

Bodalska²,

Miranowicz³

et al. 2017

Adv Clin Exp Med

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Flavonoids, naturally occuring derivatives of 2-phenyl-benzo-γ-pyrone, are widespread in plants as coloring substances. Apigenin (4' ,5,7,-trihydroxyflavone (5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one), molecular formula C₁₅H₁₀O⁵, is a flavonoid present in many fruits and vegetables, primarily in citrus fruits, apples, parsley and celery leaves. It is also found in some medicinal plants, including chamomile flowers, thyme, oregano, peppermint, lemon balm and yarrow, as a 7-O-glycoside with anti-inflammatory and antioxidant activity. In recent years it has attracted a great deal of interest as a bioactive substance reported to have anticancer properties. According to recent literature data, apigenin is able to reduce cancer cell glucose uptake, inhibit remodeling of the extracellular matrix, inhibit cell adhesion molecules that participate in cancer progression and hinder the development of blood vessels needed by growing tumors. It is reported to protect against a wide variety of cancers. The mechanism of anticancer activity is still under investigation and further research is needed.

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Silencing of CD133 inhibits GLUT1‐mediated glucose transport through downregulation of the HER3/Akt/mTOR pathway in colon cancer

Kim

Son

et al. 2019

FEBS Letters

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Cluster of differentiation 133 (CD133) is a transmembrane glycoprotein that has been reported as a marker of cancer stem cells or cancer‐initiating cells in various cancers. However, its contribution to tumorigenesis and differentiation remains to be elucidated. To determine the role of CD133 in colon cancer, we silenced CD133 in human colon cancer cells. Silencing of CD133 results in decreased cell proliferation, survival, migration, invasion, and glucose transport. These effects are mediated by downregulation of the human epidermal growth factor receptor 3 (HER3)/Akt/mTOR signaling pathway, culminating in reduced expression of the glucose transporter GLUT1. We also confirm that the cellular phenotypes of CD133‐silenced cells are mediated by GLUT1 downregulation. We conclude that CD133 is a potential tumor initiator that positively regulates GLUT1 expression through modulation of HER3/Akt/mTOR signaling.

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Apigenin Inhibits the GLUT-1 Glucose Transporter and the Phosphoinositide 3-Kinase/Akt Pathway in Human Pancreatic Cancer Cells

Cited by 136 publications

References 22 publications

Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

Recurrent prognostic factors and expression of GLUT-1, PI3K and p-Akt in adenoid cystic carcinomas of the head and neck: Clinicopathological features and biomarkers of adenoid cystic carcinoma

Insights into novel anticancer applications for apigenin

Silencing of CD133 inhibits GLUT1‐mediated glucose transport through downregulation of the HER3/Akt/mTOR pathway in colon cancer

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