Cytokinesis arrest and multiple centrosomes in B cell chronic lymphocytic leukaemia

Rogne, Marie; Svaerd, Oksana; Madsen‐Østerbye, Julia; Hashim, Adnan; Tjønnfjord, Geir E.; Staerk, Judith

doi:10.1111/jcmm.13579

Cited by 2 publications

(2 citation statements)

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“…Qu et al [79] detected the up-regulated expression of P21 as well as the down-regulated expression of cyclin E, demonstrating the molecular mechanism underlying ING4-induced G 1 arrest in colorectal LoVo cells. A recent study in chronic lymphocytic leukemia cells indicates that the altered expression level of ING4 contributes to regulation of the cell cycle, thereby disrupting mitosis [76]. Nevertheless, some studies have failed to show any relevant effect of ING4 in some cell lines [5,52].…”

Section: Dysregulation Of Ing4 In Tumors and Mechanisms Of Tumor Suppmentioning

confidence: 99%

The essential role of tumor suppressor gene ING4 in various human cancers and non-neoplastic disorders

Cheng

2019

Bioscience Reports

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Inhibitor of growth 4 (ING4), a member of the ING family discovered in 2003, has been shown to act as a tumor suppressor and is frequently down-regulated in various human cancers. Numerous published in vivo and in vitro studies have shown that ING4 is responsible for important cancer hallmarks such as pathologic cell cycle arrest, apoptosis, autophagy, contact inhibition, and hypoxic adaptation, and also affects tumor angiogenesis, invasion, and metastasis. These characteristics are typically associated with regulation through chromatin acetylation by binding histone H3 trimethylated at lysine 4 (H3K4me3) and through transcriptional activity of transcription factor P53 and NF-κB. In addition, emerging evidence has indicated that abnormalities in ING4 expression and function play key roles in non-neoplastic disorders. Here, we provide an overview of ING4-modulated chromosome remodeling and transcriptional function, as well as the functional consequences of different genetic variants. We also present the current understanding concerning the role of ING4 in the development of neoplastic and non-neoplastic diseases. These studies offer inspiration for pursuing novel therapeutics for various cancers.

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Section: Dysregulation Of Ing4 In Tumors and Mechanisms Of Tumor Suppmentioning

confidence: 99%

The essential role of tumor suppressor gene ING4 in various human cancers and non-neoplastic disorders

Cheng

2019

Bioscience Reports

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“…Interestingly, active Ras was in one study reported to induce cytokinesis in non-adherent human fibroblasts, as analyzed by FACS [16]. Because of the difficulty in analyzing bi-nucleated cells at the cytokinesis stage using FACS without breaking the narrow cytoplasmic bridge [17, 18] uncertainty still remains regarding the ability of oncogenic RAS to promote ESCRT III-mediated abscission in detached cells. In the present study we aimed to clarify this important issue, as well as to determine the fate of bi-nucleated cells in the following cell cycle and its dependence on p53.…”

Section: Introductionmentioning

confidence: 99%

Septin and Ras regulate cytokinetic abscission in detached cells

Gupta

Kamranvar

et al. 2019

Cell Div

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Background: Integrin-mediated adhesion is normally required for cytokinetic abscission, and failure in the process can generate potentially oncogenic tetraploid cells. Here, detachment-induced formation of oncogenic tetraploid cells was analyzed in non-transformed human BJ fibroblasts and BJ expressing SV40LT (BJ-LT) ± overactive HRas. Results:In contrast to BJ and BJ-LT cells, non-adherent BJ-LT-Ras cells recruited ALIX and CHMP4B to the midbody and divided. In detached BJ and BJ-LT cells regression of the cytokinetic furrow was suppressed by intercellular bridge-associated septin; after re-adhesion these cells divided by cytofission, however, some cells became bi-nucleated because of septin reorganization and furrow regression. Adherent bi-nucleated BJ cells became senescent in G1 with p21 accumulation in the nucleus, apparently due to p53 activation since adherent bi-nucleated BJ-LT cells passed through next cell cycle and divided into mono-nucleated tetraploids; the two centrosomes present in binucleated BJ cells fused after furrow regression, pointing to the PIDDosome pathway as a possible mechanism for the p53 activation.Conclusions: Several mechanisms prevent detached normal cells from generating tumor-causing tetraploid cells unless they have a suppressed p53 response by viruses, mutation or inflammation. Importantly, activating Ras mutations promote colony growth of detached transformed cells by inducing anchorage-independent cytokinetic abscission in single cells.

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Cytokinesis arrest and multiple centrosomes in B cell chronic lymphocytic leukaemia

Cited by 2 publications

References 50 publications

The essential role of tumor suppressor gene ING4 in various human cancers and non-neoplastic disorders

The essential role of tumor suppressor gene ING4 in various human cancers and non-neoplastic disorders

Septin and Ras regulate cytokinetic abscission in detached cells

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