Licensing of DNA replication, cancer, pluripotency and differentiation: An interlinked world?

Tsaniras, Spyridon Champeris; Kanellakis, Nikolaos I.; Symeonidou, Ioanna-Eleni; Nikolopoulou, Pinelopi A; Lygerou, Zoi; Taraviras, Stavros

doi:10.1016/j.semcdb.2014.03.013

Cited by 75 publications

(45 citation statements)

References 129 publications

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“…Different cyclin-CDK combinations specifically determine the downstream targeted proteins that in turn promote the expression of cyclins and enzymes required for DNA replication (6). Previous studies showed that disregulation of the cell cycle components may cause the tumor cell to multiply uncontrollably, which finally leads to tumor formation (7). Importantly, therapies targeting CDK inhibitor present a favorable prospect in the treatment of a variety of cancers.…”

Section: Introductionmentioning

confidence: 99%

miR-150 inhibits proliferation and tumorigenicity via retarding G1/S phase transition in nasopharyngeal carcinoma

Liu

Lin

et al. 2017

International Journal of Oncology

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Cancer cells are characterized by a pathological manifestation of uncontrolled proliferation, which results in tumor formation. Therefore, it is necessary to improve understanding of the underlying mechanism of cell cycle control. Here, we report that miR-150 is downregulated in nasopharyngeal carcinoma tissues and cells. Upregulation of miR-150 suppresses nasopharyngeal carcinoma (NPC) cell proliferation and induces G1/S arrest in vitro, and inhibits tumorigenesis in vivo. Conversely, silencing miR-150 yields the opposite effect. Our results further demonstrate that miR-150 retards nasopharyngeal carcinoma cell proliferation and G1/S transition via targeting multiple cell cycle-related genes, including CCND1, CCND2, CDK2 and CCNE2. Therefore, our results uncover a novel mechanistic understanding of miR-150-mediated tumor suppression in NPC, which will facilitate the development of effective cancer therapies against nasopharyngeal carcinoma.

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Section: Introductionmentioning

confidence: 99%

miR-150 inhibits proliferation and tumorigenicity via retarding G1/S phase transition in nasopharyngeal carcinoma

Liu

Lin

et al. 2017

International Journal of Oncology

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“…In connection with cell growth, the cell cycle that is the series of events that take place in a cell leading to its division into two daughter cells is a vital process for development and organ renewal and is elaborately regulated by cell cycle checkpoint components. However, cancer cells abnormally proliferate by active cell division due to a dysregulation of the cell cycle components [ 20 ] . In addition, the EMT process is an important cellular mechanism by which epithelial cells lose their cell polarity and cell-cell adhesion, instead gaining an migratory and invasive mesenchymal phenotype [ 21–22 ] .…”

Section: Introductionmentioning

confidence: 99%

Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells

et al. 2017

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Bisphenol-A (BPA) has been considered as an endocrine disrupting chemical (EDC) because it can exert estrogenic properties. For bisphenol-S (BPS) and bisphenol-F (BPF) that are BPA analogs and substitutes, their risk to estrogen-dependent cancer has been reported rarely compared with the numerous cases of BPA. In this study, we examined whether BPA, BPS, and BPF can lead to the proliferation, migration, and epithelial mesenchymal transition (EMT) of MCF-7 clonal variant (MCF-7 CV) breast cancer cells expressing estrogen receptors (ERs). In a cell viability assay, BPA, BPS, and BPF significantly increased proliferation of MCF-7 CV cells compared to control (DMSO) as did 17β-estradiol (E2). In Western blotting assay, BPA, BPS, and BPF enhanced the protein expression of cell cycle progression genes such as cyclin D1 and E1. In addition, MCF-7 CV cells lost cell to cell contacts and acquired fibroblast-like morphology by the treatment of BPA, BPS, or BPF for 24 hours. In cell migration assay, BPA, BPS, and BPF accelerated the migration capability of MCF-7 CV cells as did E2. In relation with the EMT process, BPA, BPS, and BPF increased the protein expression ofN-cadherin, while they decreased the protein expression of E-cadherin. When BPA, BPS, and BPF were co-treated with ICI 182,780, an ER antagonist, proliferation effects were reversed, the expression of cyclin D1 and cyclin E1 was downregulated, and the altered cell migration and expression ofN-cadherin and E-cadherin by BPA, BPS, and BPF were restored to the control level. Thus, these results imply that BPS and BPF also have the risk of breast cancer progression as much as BPA in the induction of proliferation and migration of MCF-7 CV cells by regulating the protein expression of cell cycle-related genes and EMT markersvia the ER-dependent pathway.

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“…Dysregulation of cell cycle components may cause the cell to multiply uncontrollably, thus leading to tumor formation (Champeris Tsaniras et al, 2014), as is the case for GBM (Hazane-Puch et al, 2015;Xie et al, 2015). Various studies have shown that the cell cycle pathway and cell cycle-related molecules can be considered therapeutic targets of many cancers (Rao, 1996;Newman et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of TFDP1 and of the cell cycle pathway in high-grade glioblastoma multiforme: a bioinformatic analysis

Lü¹,

Lv²,

Yh³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Despite extensive research, the prognosis of high-grade glioblastoma multiforme (GBM) has improved only slightly because of the limited response to standard treatments. Recent advances (discoveries of molecular biomarkers) provide new opportunities for the treatment of GBM. The aim of the present study was to identify diagnostic biomarkers of high-grade GBM. First, we combined 3 microarray expression datasets to screen them for genes differentially expressed in patients with high-grade GBM relative to healthy subjects. Next, the target network was constructed via the empirical Bayesian coexpression approach, and centrality analysis and a molecular complex detection (MCODE) algorithm were performed to explore hub genes and functional modules. Finally, a validation test was conducted to verify the bioinformatic results. A total of 277 differentially expressed genes were identified according to the criteria P < 0.05 and |log 2 (fold change)| ≥ 1.5. These genes were most significantly enriched in the cell cycle pathway. Centrality analysis uncovered 9 hub genes; among them, TFDP1 showed the highest degree of connectivity (43) and is a known participant in the cell cycle pathway; this finding pointed to the important role of TFDP1 in the progression of high-grade GBM. Experimental validation mostly supported the bioinformatic results. According to our study results, the gene TFDP1 and the cell cycle pathway are strongly associated with high-grade GBM; this result may provide new insights into the pathogenesis of GBM.

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Licensing of DNA replication, cancer, pluripotency and differentiation: An interlinked world?

Cited by 75 publications

References 129 publications

miR-150 inhibits proliferation and tumorigenicity via retarding G1/S phase transition in nasopharyngeal carcinoma

miR-150 inhibits proliferation and tumorigenicity via retarding G1/S phase transition in nasopharyngeal carcinoma

Effects of bisphenol compounds on the growth and epithelial mesenchymal transition of MCF-7 CV human breast cancer cells

Dysregulation of TFDP1 and of the cell cycle pathway in high-grade glioblastoma multiforme: a bioinformatic analysis

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