Akt is involved in the inhibition of cell proliferation by EGF

Jeon, Soung Hoo; Jeong, Woo-Jeong; Cho, Jae-Young; Lee, Kee-Ho; Choi, Kang‐Yell

doi:10.1038/emm.2007.54

Cited by 5 publications

(3 citation statements)

References 44 publications

(56 reference statements)

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“…The P13K and ERK are too triggered by Wnt3a, and that is allied with cellular propagation [54, 55]. Auxiliary numerous observations have been confirmed control of the RAF-1-MEK-ERK signaling cascade by the Wnt/β-catenin signaling [56–58]. Additionally, GSK3β, chief player of Wnt/β-catenin pathway, is controlled by RAS-MAPK and PI3 K-Akt signaling cascades, and the cross-talk between GSK3β and RAS-MAPK or PI3K/AKT/mTOR signaling pathways is implicated in the pathogenesis of HCC and pancreatic cancer [59, 60].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): involvement of Wnt/β-catenin and other signal transduction pathways

et al. 2019

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BackgroundMore than the two decades, the question of whether vitamin D has a role in cancer frequency, development, and death has been premeditated in detail. Colorectal, breast, and prostate cancers have been a scrupulous spot of center, altogether, these three malignancies report for approximately 35% of cancer cases and 20% of cancer demises in the United States, and as such are a chief public health apprehension. The aim was to evaluate antitumor activity of Vitamin D-Nanoemulsion (NVD) in colorectal cancer cell lines and HCT116 xenograft model in a comprehensive approach.MethodsTwo human colorectal cancer cell lines HCT116 and HT29 (gained from College of Pharmacy, King Saud University, KSA were grown. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazoliumbromide protocol were performed to show the impact of NVD and β-catenin inhibitor (FH535) on the viability of HCT116 and HT29 cell lines. Apoptosis/cell cycle assay was performed. Analysis was done with a FACScan (Becton–Dickinson, NJ). About 10,000 cells per sample were harvested and Histograms of DNA were analyzed with ModiFitLT software (verity Software House, ME, USA). Western blotting and RT-PCR were performed for protein and gene expression respectively in in vitro and in vivo.ResultsWe found that NVD induced cytotoxicity in colorectal cells in a dose-dependent manner and time dependent approach. Further, our data validated that NVD administration of human colorectal cancer HCT116 and HT29 cells resulted in cell growth arrest, alteration in molecules regulating cell cycle operative in the G2 phase of the cell cycle and apoptosis in a dose dependent approach. Further our results concluded that NVD administration decreases expression of β-catenin gene, AKT gene and Survivin gene and protein expression in in vitro and in vivo.ConclusionOur findings suggest that targeting β-catenin gene may encourage the alterations of cell cycle and cell cycle regulators. Wnt/β-catenin signaling pathway possibly takes part in the genesis and progression of colorectal cancer cells through regulating cell cycle and the expression of cell cycle regulators.Electronic supplementary materialThe online version of this article (10.1186/s13578-019-0277-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): involvement of Wnt/β-catenin and other signal transduction pathways

et al. 2019

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“…Recent published data show that the connecting link between the two pathways is Axin, a negative regulator of the canonic Wnt pathway/␤-catenin signaling pathway, 22 which is responsible for downregulation of ␤-catenin signaling, acting in a negative feedback loop via Akt. 23,24 Our data showed that incubation of cells in EGF resulted in a decrease in ␤-catenin and GSK-3␤ transcription and translation comparable to IGF-1 data.…”

Section: Discussionmentioning

confidence: 99%

Activation of the β-Catenin Signaling Pathway and Its Impact on RPE Cell Cycle

Steindl-Kuscher

Krugluger

Boulton

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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“…For example, activation of the MEK/ERK 1/2 cascade regulated fibroblast proliferation induced by insulin growth factor-I (54) and by muscarinic receptor stimulation (47). Other authors showed the activation of both the MEK/ ERK pathway and the PI3K/Akt pathway in fibroblast proliferation stimulated with ionizing radiation (37) or EGF (31). Moreover, the PI3K-Akt pathway mediates growth and proliferation induced by Wnt3a protein in NIH3T3 (39) and in renal fibroblasts (79).…”

Section: Discussionmentioning

confidence: 99%

H-Ras isoform modulates extracellular matrix synthesis, proliferation, and migration in fibroblasts

Fuentes-Calvo

Blázquez‐Medela

Eleno

et al. 2012

American Journal of Physiology-Cell Physiology

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Ras GTPases are ubiquitous plasma membrane transducers of extracellular stimuli. In addition to their role as oncogenes, Ras GTPases are key regulators of cell function. Each of the Ras isoforms exhibits specific modulatory activity on different cellular pathways. This has prompted researchers to determine the pathophysiological roles of each isoform. There is a proven relationship between the signaling pathways of transforming growth factor-β1 (TGF-β1) and Ras GTPases. To assess the individual role of H-Ras oncogene in basal and TGF-β1-mediated extracellular matrix (ECM) synthesis, proliferation, and migration in fibroblasts, we analyzed these processes in embryonic fibroblasts obtained from H-Ras knockout mice ( H-ras−/−). We found that H- ras−/− fibroblasts exhibited a higher basal phosphatidylinositol-3-kinase (PI3K)/Akt activation than wild-type (WT) fibroblasts, whereas MEK/ERK 1/2 activation was similar in both types of cells. Fibronectin and collagen synthesis were higher in H -ras−/− fibroblasts and proliferation was lower in H -ras−/− than in WT fibroblasts. Moreover, H-Ras appeared indispensable to maintain normal fibroblast motility, which was highly restricted in H- ras−/− cells. These results suggest that H-Ras (through downregulation of PI3K/Akt activation) could modulate fibroblast activity by reducing ECM synthesis and upregulating both proliferation and migration. TGF-β1 strongly increased ERK and Akt activation in WT but not in H- ras−/− fibroblasts, suggesting that H-Ras is necessary to increase ERK 1/2 activation and to maintain PI3K downregulation in TGF-β1-stimulated fibroblasts. TGF-β1 stimulated ECM synthesis and proliferation, although ECM synthesis was higher and proliferation lower in H- ras−/− than in WT fibroblasts. Hence, H-Ras activation seems to play a key role in the regulation of these effects.

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Akt is involved in the inhibition of cell proliferation by EGF

Cited by 5 publications

References 44 publications

RETRACTED ARTICLE: Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): involvement of Wnt/β-catenin and other signal transduction pathways

RETRACTED ARTICLE: Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): involvement of Wnt/β-catenin and other signal transduction pathways

Activation of the β-Catenin Signaling Pathway and Its Impact on RPE Cell Cycle

H-Ras isoform modulates extracellular matrix synthesis, proliferation, and migration in fibroblasts

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