http://www.celldiv.com The most accessed research articles published by Cell Division 2011-12-28T00:00:00Z Increasing knowledge on the cell cycle deregulations in cancers has promoted the introduction of phytochemicals, which can either modulate signaling pathways leading to cell cycle regulation or directly alter cell cycle regulatory molecules, in cancer therapy. Most human malignancies are driven by chromosomal translocations or other genetic alterations that directly affect the function of critical cell cycle proteins such as cyclins as well as tumor suppressors, e.g., p53. In this respect, cell cycle regulation and its modulation by curcumin are gaining widespread attention in recent years. Extensive research has addressed the chemotherapeutic potential of curcumin (diferuloylmethane), a relatively non-toxic plant derived polyphenol. The mechanisms implicated are diverse and appear to involve a combination of cell signaling pathways at multiple levels. In the present review we discuss how alterations in the cell cycle control contribute to the malignant transformation and provide an overview of how curcumin targets cell cycle regulatory molecules to assert anti-proliferative and/or apoptotic effects in cancer cells. The purpose of the current article is to present an appraisal of the current level of knowledge regarding the potential of curcumin as an agent for the chemoprevention of cancer via an understanding of its mechanism of action at the level of cell cycle regulation. Taken together, this review seeks to summarize the unique properties of curcumin that may be exploited for successful clinical cancer prevention. http://www.celldiv.com/content/3/1/14 Gaurisankar Sa Tanya Das Cell Division 2008, null:14 2008-10-03T00:00:00Z doi:10.1186/1747-1028-3-14 /content/figures/1747-1028-3-14-toc.gif Cell Division 1747-1028 ${item.volume} 14 2008-10-03T00:00:00Z XML The cyclin dependent kinase Cdk1 controls the cell cycle, which is best understood in the model organism S. cerevisiae. Research performed during the past decade has significantly improved our understanding of the molecular machinery of the cell cycle. Approximately 75 targets of Cdk1 have been identified that control critical cell cycle events, such as DNA replication and segregation, transcriptional programs and cell morphogenesis. In this review we discuss currently known targets of Cdk1 in the budding yeast S. cerevisiae and highlight the role of Cdk1 in several crucial processes including maintenance of genome stability. http://www.celldiv.com/content/5/1/11 Jorrit Enserink Richard Kolodner Cell Division 2010, null:11 2010-05-13T00:00:00Z doi:10.1186/1747-1028-5-11 /content/figures/1747-1028-5-11-toc.gif Cell Division 1747-1028 ${item.volume} 11 2010-05-13T00:00:00Z XML Inflammation is an important environmental factor that promotes tumourigenesis and the progression of established cancerous lesions, and recent studies have started to dissect the mechanisms linking the two pathologies. These inflammatory and infectious conditions trigger immune and stromal cell release of soluble mediators which facilitate survival and proliferation of tumour cells in a paracrine manner. In addition, (epi-)genetic mutations affecting oncogenes, tumour-suppressor genes, chromosomal rearrangements and amplifications trigger the release of inflammatory mediators within the tumour microenvironment to promote neoplastic growth in an autocrine manner. These two pathways converge in tumour cells and result in activation of the latent signal transducer and activator of transcription 3 (Stat3) which mediates a transcriptional response favouring survival, proliferation and angiogenesis. The abundance of cytokines that activate Stat3 within the tumour microenvironment, which comprises of members of the interleukin (IL) IL6, IL10 and IL17/23 families, underpins a signaling network that simultaneously promotes the growth of neoplastic epithelium, fuels inflammation and suppresses the host's anti-tumour immune response. Accordingly, aberrant and persistent Stat3 activation is a frequent observation in human cancers of epithelial origin and is often associated with poor outcome.Here we summarize insights gained from mice harbouring mutations in components of the Stat3 signaling cascade and in particular of gp130, the shared receptor for the IL6 family of cytokines. We focus on the various feed-back and feed-forward loops in which Stat3 provides the signaling node in cells of the tumour and its microenvironment thereby functionally linking excessive inflammation to neoplastic growth. Although these observations are particularly pertinent to gastrointestinal tumours, we suggest that the tumour's addiction to persistent Stat3 activation is likely to also impact on other epithelial cell-derived cancers. These insights provide clues to the judicious interference of the gp130/Stat3 signaling cascade in therapeutically targeting cancer. http://www.celldiv.com/content/5/1/14 Andrew Jarnicki Tracy Putoczki Matthias Ernst Cell Division 2010, null:14 2010-05-17T00:00:00Z doi:10.1186/1747-1028-5-14 /content/figures/1747-1028-5-14-toc.gif Cell Division 1747-1028 ${item.volume} 14 2010-05-17T00:00:00Z XML Cell Division is a new, open access, peer-reviewed online journal that publishes cutting-edge articles, commentaries and reviews on all exciting aspects of cell cycle control in eukaryotes. A major goal of this new journal is to publish timely and significant studies on the aberrations of the cell cycle network that occur in cancer and other diseases. http://www.celldiv.com/content/1/1/1 Philipp Kaldis Michele Pagano Cell Division 2006, null:1 2006-04-03T00:00:00Z doi:10.1186/1747-1028-1-1 /content/figures/1747-1028-1-1-toc.gif Cell Division 1747-1028 ${item.volume} 1 2006-04-03T00:00:00Z XML No description available http://www.celldiv.com/content/2/1/27 Mignon Keaton Cell Division 2007, null:27 2007-09-17T00:00:00Z doi:10.1186/1747-1028-2-27 /content/figures/1747-1028-2-27-toc.gif Cell Division 1747-1028 ${item.volume} 27 2007-09-17T00:00:00Z XML Senescence and mitotic catastrophe (MC) are two distinct crucial non-apoptotic mechanisms, often triggered in cancer cells and tissues in response to anti-cancer drugs. Chemotherapeuticals and myriad other factors induce cell eradication via these routes. While senescence drives the cells to a state of quiescence, MC drives the cells towards death during the course of mitosis. The senescent phenotype distinguishes tumor cells that survived drug exposure but lost the ability to form colonies from those that recover and proliferate after treatment. Although senescent cells do not proliferate, they are metabolically active and may secrete proteins with potential tumor-promoting activities. The other anti-proliferative response of tumor cells is MC that is a form of cell death that results from abnormal mitosis and leads to the formation of interphase cells with multiple micronuclei. Different classes of cytotoxic agents induce MC, but the pathways of abnormal mitosis differ depending on the nature of the inducer and the status of cell-cycle checkpoints. In this review, we compare the two pathways and mention that they are activated to curb the growth of tumors. Altogether, we have highlighted the possibilities of the use of senescence targeting drugs, mitotic kinases and anti-mitotic agents in fabricating novel strategies in cancer control. http://www.celldiv.com/content/5/1/4 Richa Singh Jasmine George Yogeshwer Shukla Cell Division 2010, null:4 2010-01-21T00:00:00Z doi:10.1186/1747-1028-5-4 /content/figures/1747-1028-5-4-toc.gif Cell Division 1747-1028 ${item.volume} 4 2010-01-21T00:00:00Z XML Background: Cdc5 (polo kinase/Plk1) is a highly conserved key regulator of the S. cerevisiae cell cycle from S-phase until cytokinesis. However, much of the regulatory mechanisms that govern Cdc5 remain to be determined. Cdc5 is phosphorylated on up to 10 sites during mitosis. In this study, we investigated the function of phosphorylation site T23, the only full consensus Cdk1 (Cdc28) phosphorylation site present.FindingsCdc5T23A introduces a degron that reduces its cellular amount to undetectable levels, which are nevertheless sufficient for normal cell proliferation. The degron acts in cis and is reversed by N-terminal GFP-tagging. Cdk1 kinase activity is required to maintain Cdc5 levels during G2. This, Cdk1 inhibited, Cdc5 degradation is APC/CCdh1 independent and requires new protein synthesis. Cdc5T23E is hyperactive, and reduces the levels of Cdc5 (in trans) and drastically reduces Clb2 levels. Conclusions: Phosphorylation of Cdc5 by Cdk1 is required to maintain Cdc5 levels during G2. However, phosphorylation of T23 (probably by Cdk1) caps Cdc5 and other CLB2 cluster protein accumulation, preventing potential protein toxicity, which may arise from their overexpression or from APC/CCdh1 inactivation. http://www.celldiv.com/content/6/1/23 Kobi Simpson-Lavy Michael Brandeis Cell Division 2011, null:23 2011-12-28T00:00:00Z doi:10.1186/1747-1028-6-23 /content/figures/1747-1028-6-23-toc.gif Cell Division 1747-1028 ${item.volume} 23 2011-12-28T00:00:00Z XML Monoubiquitination of H2A is a major histone modification in mammalian cells. Understanding how monoubiquitinated H2A (uH2A) regulates DNA-based processes in the context of chromatin is a challenging question. Work in the past years linked uH2A to transcriptional repression by the Polycomb group proteins of developmental regulators. Recently, a number of mammalian deubiquitinating enzymes (DUBs) that catalyze the removal of ubiquitin from H2A have been discovered. These studies provide convincing evidence that H2A deubiquitination is connected with gene activation. In addition, uH2A regulatory enzymes have crucial roles in the cellular response to DNA damage and in cell cycle progression. In this review we will discuss new insights into uH2A biology, with emphasis on the H2A DUBs. http://www.celldiv.com/content/3/1/8 Joseph Vissers Francesco Nicassio Maarten van Lohuizen Pier Paolo Di Fiore Elisabetta Citterio Cell Division 2008, null:8 2008-04-22T00:00:00Z doi:10.1186/1747-1028-3-8 /content/figures/1747-1028-3-8-toc.gif Cell Division 1747-1028 ${item.volume} 8 2008-04-22T00:00:00Z XML Background: Multicellular tumor spheroids are models of increasing interest for cancer and cell biology studies. They allow considering cellular interactions in exploring cell cycle and cell division mechanisms. However, 3D imaging of cell division in living spheroids is technically challenging and has never been reported. Results: Here, we report a major breakthrough based on the engineering of multicellular tumor spheroids expressing an histone H2B fluorescent nuclear reporter protein, and specifically designed sample holders to monitor live cell division dynamics in 3D large spheroids using an home-made selective-plane illumination microscope. Conclusions: As illustrated using the antimitotic drug, paclitaxel, this technological advance paves the way for studies of the dynamics of cell divion processes in 3D and more generally for the investigation of tumor cell population biology in integrated system as the spheroid model. http://www.celldiv.com/content/6/1/22 Corinne Lorenzo Celine Frongia Raphael Jorand Jerome Fehrenbach Pierre Weiss Amina Maandhui Guillaume Gay Bernard Ducommun Valerie Lobjois Cell Division 2011, null:22 2011-12-12T00:00:00Z doi:10.1186/1747-1028-6-22 Imaging and 3D reconstruction of interphase and mitotic nuclei within a fixed H2B¿HcRed-expressing spheroid Picture illustrating 3D reconstructions of interphase and mitotic nuclei within a fixed H2B¿HcRed-expressing spheroid. The blue correspond to interphase nuclei and red to mitotic condensed chromosomes. These reconstructions have been obtained from SPIM z-stacks and processed using the VSNR, FIJI and Imaris softwares. /content/figures/1747-1028-6-22-toc.gif Cell Division 1747-1028 ${item.volume} 22 2011-12-12T00:00:00Z PDF The anaphase promoting complex/cyclosome (APC/C) is a multi-subunit E3 ubiquitin ligase playing essential functions in mitosis. It is conserved from yeast to human and relies on two adaptor proteins, Cdc20 and Cdh1, to bring in substrates. Both APCCdc20 and APCCdh1 are implicated in the control of mitosis through mediating ubiquitination and degradation of important mitotic regulators such as cyclin B1, securin, and Plk1. In addition, APCCdh1 is thought to prevent premature S phase entry by limiting the accumulation of mitotic cyclins in G1 and to regulate processes unrelated to cell cycle. In this review, we will summarize our current understanding of APCCdh1 function in cell cycle and beyond. http://www.celldiv.com/content/4/1/2 Min Li Pumin Zhang Cell Division 2009, null:2 2009-01-19T00:00:00Z doi:10.1186/1747-1028-4-2 /content/figures/1747-1028-4-2-toc.gif Cell Division 1747-1028 ${item.volume} 2 2009-01-19T00:00:00Z XML