Signaling Pathways that Control Cell Proliferation

Duronio, Robert J.; Xiong, Yue

doi:10.1101/cshperspect.a008904

Cited by 307 publications

(248 citation statements)

References 118 publications

(110 reference statements)

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“…If the protein levels of cyclin A and B do not increase after G 1 phase, cell progression cannot pass through G 2 /M phase and complete mitosis. 28 In the present work, following CuONP treatment, the deregulation of cyclin A and B dynamics led to blockage of G 2 /M transitions and further promoted viability loss (Figures 2 and 3).…”

Section: Discussionmentioning

confidence: 94%

Activation of Erk and p53 regulates copper oxide nanoparticle-induced cytotoxicity in keratinocytes and fibroblasts

Luo¹,

Li²,

Yang³

et al. 2014

IJN

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Copper oxide nanoparticles (CuONP) have attracted increasing attention due to their unique properties and have been extensively utilized in industrial and commercial applications. For example, their antimicrobial capability endows CuONP with applications in dressings and textiles against bacterial infections. Along with the wide applications, concerns about the possible effects of CuONP on humans are also increasing. It is crucial to evaluate the safety and impact of CuONP on humans, and especially the skin, prior to their practical application. The potential toxicity of CuONP to skin keratinocytes has been reported recently. However, the underlying mechanism of toxicity in skin cells has remained unclear. In the present work, we explored the possible mechanism of the cytotoxicity of CuONP in HaCaT human keratinocytes and mouse embryonic fibroblasts (MEF). CuONP exposure induced viability loss, migration inhibition, and G 2 /M phase cycle arrest in both cell types. CuONP significantly induced mitogen-activated protein kinase (extracellular signal-regulated kinase [Erk], p38, and c-Jun N-terminal kinase [JNK]) activation in dose- and time-dependent manners. U0126 (an inhibitor of Erk), but not SB 239063 (an inhibitor of p38) or SP600125 (an inhibitor of JNK), enhanced CuONP-induced viability loss. CuONP also induced decreases in p53 and p-p53 levels in both cell types. Cyclic pifithrin-α, an inhibitor of p53 transcriptional activity, enhanced CuONP-induced viability loss. Nutlin-3α, a p53 stabilizer, prevented CuONP-induced viability loss in HaCaT cells, but not in MEF cells, due to the inherent toxicity of nutlin-3α to MEF. Moreover, the experiments on primary keratinocytes are in accordance with the conclusions acquired from HaCaT and MEF cells. These data demonstrate that the activation of Erk and p53 plays an important role in CuONP-induced cytotoxicity, and agents that preserve Erk or p53 activation may prevent CuONP-induced cytotoxicity.

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Section: Discussionmentioning

confidence: 94%

Activation of Erk and p53 regulates copper oxide nanoparticle-induced cytotoxicity in keratinocytes and fibroblasts

Luo¹,

Li²,

Yang³

et al. 2014

IJN

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“…Cell cycle progression is directly driven by a series of heterodimers formed by cyclins and cyclin-dependent kinases (CDKs) [18]. The decision for a cell to enter S phase is tightly controlled by cyclin D/CDK4/6 and cyclin E/CDK2 complexes, followed by cyclin A/CDK2 throughout S phase [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

et al. 2014

Cell Communication and Signaling

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Background: Accelerated cell cycle progression is the common feature of most cancers. MiRNAs can act as oncogenes or tumor suppressors by directly modulating cell cycle machinery. It has been shown that miR-188 is upregulated in UVB-irradiated mouse skin and human nasopharyngeal carcinoma CNE cells under hypoxic stress. However, little is known about the function of miR-188 in cell proliferation and growth control. Results: Overexpression of miR-188 inhibits cell proliferation, tumor colony formation and G 1 /S cell cycle transition in human nasopharyngeal carcinoma CNE cells. Using bioinformatics approach, we identify a series of genes regulating G 1 /S transition as putative miR-188 targets. MiR-188 inhibits both mRNA and protein expression of CCND1, CCND3, CCNE1, CCNA2, CDK4 and CDK2, suppresses Rb phosphorylation and downregulates E2F transcriptional activity. The expression level of miR-188 also inversely correlates with the expression of miR-188 targets in human nasopharyngeal carcinoma (NPC) tissues. Moreover, studies in xenograft mouse model reveal that miR-188 is capable of inhibiting tumor initiation and progression by suppressing target genes expression and Rb phosphorylation.

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“…Cyclins have five major classes (cyclin A, B, C, D1-3 and E) [5] and CDKs family composed mainly of CDK 1, 2, 4 and 6; each phase of cell cycle has specific types of cyclin/CDK complexes which responsible for proper regulation of this phase [6].…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Expression of Cyclin D1 in Invasive Ductal Carcinoma of Human Breast

Assem¹,

Youssef²,

Rashad³

et al. 2017

Oncomedicine

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Cyclin D1 has been observed in many human tumors and is likely to promote cell proliferation and differentiation by shortening the G1/S transition. This work was aimed to evaluate the prognostic role of Cyclin D1 in invasive ductal carcinoma (IDC) and its correlation with other established prognostic parameters of breast cancer. This study was conducted on 40 prospective biopsies taken from patients with breast tumor; 30 cases having IDC and 10 cases with benign tumor as well as 10 normal biopsies. Sections from all cases were subjected to stain with haematoxylin and eosin (H&E) for histopathological examination and immunohistochemical technique for Cyclin D1 in addition using flow cytometric technique to perform cell cycle analysis. Histopathological results showed fibroadenoma and fibrocystic disease in benign cases and IDC with 60% grade II and 40% grade III in malignant cases. Immunohistochemical results revealed higher expression of Cyclin D1 in IDC comparing to normal and benign breast tissues. Statistically there was significant correlation between Cyclin D1 scores and the positivity of estrogen receptor (ER) and progesterone receptor (PR), and no significant correlation was seen between Cyclin D1 and S-phase %. It could be suggested that Cyclin D1 protein may be a valuable prognostic marker in IDC and can be targeted in the future therapeutic approaches.

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Signaling Pathways that Control Cell Proliferation

Cited by 307 publications

References 118 publications

Activation of Erk and p53 regulates copper oxide nanoparticle-induced cytotoxicity in keratinocytes and fibroblasts

Activation of Erk and p53 regulates copper oxide nanoparticle-induced cytotoxicity in keratinocytes and fibroblasts

MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

Immunohistochemical Expression of Cyclin D1 in Invasive Ductal Carcinoma of Human Breast

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