Mécanismes moléculaires contrôlant le cycle cellulaire : aspects fondamentaux et implications en cancérologie

Viallard, J.F.; Lacombe, Francis; Belloc, Françis; Pellegrin, Jean‐Luc; Reiffers, J.

doi:10.1016/s1278-3218(01)00087-7

Cited by 81 publications

(26 citation statements)

References 162 publications

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“…Cell cycle is regulated by an intricate network of cyclin/CDK complexes. Amongst the , G 2 cyclins', CCNB1 forms a complex with CDK1 and is involved in the control of the G 2 /M transition and mitosis [32]. The data presented here show that the G 2 /M arrest observed in Caco-2 cells exposed to the mixture of EA and urolithins is associated with the downregulation of CCNB1, both at the mRNA and protein levels.…”

Section: Discussionmentioning

confidence: 59%

Gene expression, cell cycle arrest and MAPK signalling regulation in Caco‐2 cells exposed to ellagic acid and its metabolites, urolithins

González‐Sarrías

Espı́n

Tomás-Barberán

et al. 2009

Molecular Nutrition Food Res

141

105

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Novel gene expression profiles and cellular functions modulated in Caco-2 cells in response to the dietary polyphenol, ellagic acid (EA), and its colonic metabolites, urolithin-A (3,8-dihydroxy-6H-dibenzo[b,d] pyran-6-one) and urolithin-B (3-hydroxy-6H-dibenzo[b,d] pyran-6-one) have been identified. Exposure of cells to EA and urolithins arrested cell growth at the S- and G(2)/M-phases. Transcriptional profiling using microarray and functional analysis revealed changes in the expression levels of MAPK signalling genes such as, growth factor receptors (FGFR2, EGFR), oncogenes (K-Ras, c-Myc), and tumour suppressors (DUSP6, Fos) and of genes involved in cell cycle (CCNB1, CCNB1IP1). Results suggest that EA and urolithin-A and -B, at concentrations achievable in the lumen from the diet, might contribute to colon cancer prevention by modulating the expression of multiple genes in epithelial cells lining the colon. Some of these genes are involved in key cellular processes associated with cancer development and are currently being investigated as potential chemopreventive targets.

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Section: Discussionmentioning

confidence: 59%

Gene expression, cell cycle arrest and MAPK signalling regulation in Caco‐2 cells exposed to ellagic acid and its metabolites, urolithins

González‐Sarrías

Espı́n

Tomás-Barberán

et al. 2009

Molecular Nutrition Food Res

141

105

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“…In agreement with this, EGCG-MP attenuated the expression of STAT3-related survival genes such as Bcl-2, Bcl-xL, Mcl-1 and survivin in K562 cells. A variety of cellular responses are elicited by cell cycle-related genes (Viallard et al, 2001;Nixon et al, 2005). Here, EGCG-MP attenuated the expression of cell cycle-associated genes such as cyclin D1 and cyclin E, Cdk4 and activated the cyclin D1 inhibitor p21 (Chassot et al, 2008) in K562 cells, indicating that the regulation of cell cycle genes is critically involved in EGCG-MP induced cell death in K562 cells.…”

Section: Figurementioning

confidence: 86%

A derivative of epigallocatechin‐3‐gallate induces apoptosis via SHP‐1‐mediated suppression of BCR‐ABL and STAT3 signalling in chronic myelogenous leukaemia

Jung

Yun

Choo

et al. 2015

British J Pharmacology

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Background and PurposeEpigallocatechin‐3‐gallate (EGCG) is a component of green tea known to have chemo‐preventative effects on several cancers. However, EGCG has limited clinical application, which necessitates the development of a more effective EGCG prodrug as an anticancer agent.Experimental ApproachDerivatives of EGCG were evaluated for their stability and anti‐tumour activity in human chronic myeloid leukaemia (CML) K562 and KBM5 cells.Key ResultsEGCG‐mono‐palmitate (EGCG‐MP) showed most prolonged stability compared with other EGCG derivatives. EGCG‐MP exerted greater cytotoxicity and apoptosis in K562 and KBM5 cells than the other EGCG derivatives. EGCG‐MP induced Src‐homology 2 domain‐containing tyrosine phosphatase 1 (SHP‐1) leading decreased oncogenic protein BCR‐ABL and STAT3 phosphorylation in CML cells, compared with treatment with EGCG. Furthermore, EGCG‐MP reduced phosphorylation of STAT3 and survival genes in K562 cells, compared with EGCG. Conversely, depletion of SHP‐1 or application of the tyrosine phosphatase inhibitor pervanadate blocked the ability of EGCG‐MP to suppress phosphorylation of BCR‐ABL and STAT3, and the expression of survival genes downstream of STAT3. In addition, EGCG‐MP treatment more effectively suppressed tumour growth in BALB/c athymic nude mice compared with untreated controls or EGCG treatment. Immunohistochemistry revealed increased caspase 3 and SHP‐1 activity and decreased phosphorylation of BCR‐ABL in the EGCG‐MP‐treated group relative to that in the EGCG‐treated group.Conclusions and ImplicationsEGCG‐MP induced SHP‐1‐mediated inhibition of BCR‐ABL and STAT3 signalling in vitro and in vivo more effectively than EGCG. This derivative may be a potent chemotherapeutic agent for CML treatment.

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“…Higher expression of TGF-␤ and p21 readily explains the decreased proliferation of NFI-C Ϫ/Ϫ keratinocyte progenitor cells at the onset of anagen, as TGF-␤ is known to inhibit epithelial cell growth and to ellicit a p21-mediated arrest of cells in the G 1 phase of the cell cycle (45,57). However, it has been recently shown that Smad4 Ϫ/Ϫ mice display a depletion of stem cells during the first hair follicle cycles (52).…”

Section: Discussionmentioning

confidence: 99%

Nuclear Factor I-C Regulates TGF-β-dependent Hair Follicle Cycling*

Plasari

Edelmann

Hogger

et al. 2010

Journal of Biological Chemistry

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Mécanismes moléculaires contrôlant le cycle cellulaire : aspects fondamentaux et implications en cancérologie

Cited by 81 publications

References 162 publications

Gene expression, cell cycle arrest and MAPK signalling regulation in Caco‐2 cells exposed to ellagic acid and its metabolites, urolithins

Gene expression, cell cycle arrest and MAPK signalling regulation in Caco‐2 cells exposed to ellagic acid and its metabolites, urolithins

A derivative of epigallocatechin‐3‐gallate induces apoptosis via SHP‐1‐mediated suppression of BCR‐ABL and STAT3 signalling in chronic myelogenous leukaemia

Nuclear Factor I-C Regulates TGF-β-dependent Hair Follicle Cycling*

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