Heterogeneity, polyploidy, aneusomy, and 9p deletion in human glioblastoma multiforme

Park, Se Hyuck; Maeda, Tatsuhiro; Mohapatra, Gayatry; Waldman, Frederic M.; Davis, Richard L.; Feuerstein, Burt G.

doi:10.1016/0165-4608(95)00040-v

Cited by 16 publications

(8 citation statements)

References 45 publications

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“…Polyploidy is an important characteristic of major solid tumor tissues and tumor-derived cells (Lemez et al , 1998; Lothschutz et al , 2002; Olaharski et al , 2006; Park et al , 1995; Shi and King, 2005; Takanishi et al , 1996). The data presented here demonstrate that cytokinesis failure is a primary mechanism for the increased ploidy of oral carcinoma cells and the molecular defects leading to cytokinesis failure in these and other cancer cell types.…”

Section: Discussionmentioning

confidence: 99%

“…In many cancer cells, CIN is associated with chromosomal and centrosomal amplification. Tetraploidy, or twice the normal number of chromosomes, has been observed in some cancers, such as myeloid leukemia, malignant gliomas, colonic adenocarcinoma, (Lemez et al , 1998; Park et al , 1995; Takanishi et al , 1996) and tumor-derived cell lines (Olaharski et al , 2006; Shi and King, 2005). Shackney et al have shown that one of the earliest events in human tumor formation is development of tetraploidy (Shackney et al , 1989).…”

Section: Introductionmentioning

confidence: 99%

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Deficiency in myosin light-chain phosphorylation causes cytokinesis failure and multipolarity in cancer cells

Sahasrabudhe

Luo

et al. 2010

Oncogene

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Cancer cells often have unstable genomes and increased centrosome and chromosome numbers, which play an important part of malignant transformation in the most recent models tumorigenesis. However, very little is known about divisional failures in cancer cells that may lead to chromosomal and centrosomal amplifications. We show here that cancer cells often failed at cytokinesis due to decreased phosphorylation of the myosin regulatory light chain (MLC), a key regulatory component of cortical contraction during division. Reduced MLC phosphorylation was associated with high expression of myosin phosphatase and/or reduced myosin light chain kinase levels. Furthermore, expression of phosphomimetic MLC largely prevented cytokinesis failure in the tested cancer cells. When myosin light chain phosphorylation was restored to normal levels by phosphatase knockdown multinucleation, and multipolar mitosis were both markedly reduced, resulting in enhanced genome stabilization. Furthermore, both overexpression of myosin phosphatase or inhibition of the myosin light chain kinase (MLCK) in nonmalignant cells can recapitulate some of the mitotic defects of cancer cells, including multinucleation and multipolar spindles, indicating these changes are sufficient to reproduce the cytokinesis failures we see in cancer cells. These results for the first time define the molecular defects leading to divisional failure in cancer cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Deficiency in myosin light-chain phosphorylation causes cytokinesis failure and multipolarity in cancer cells

Sahasrabudhe

Luo

et al. 2010

Oncogene

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“…Underlying genomic or chromosomal instability may stimulate the accumulation of mutations and hence CIN is regarded as the initiation point of tumorigenesis [63]. CIN has been observed in various cancers, including glioblastoma multiforme [64], cervical malignancies [65], colonic adenocarcinoma [66] and other tumor-derived cell lines [67]. In addition to CIN, divisional failures also cause chromosomal and centrosomal amplifications [61].…”

Section: Effects Of Myosins On Genetic or Chromosomal Instabilitymentioning

confidence: 99%

Myosins as fundamental components during tumorigenesis: diverse and indispensable

Yang

2016

Oncotarget

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Myosin is a kind of actin-based motor protein. As the crucial functions of myosin during tumorigenesis have become increasingly apparent, the profile of myosin in the field of cancer research has also been growing. Eighteen distinct classes of myosins have been discovered in the past twenty years and constitute a diverse superfamily. Various myosins share similar structures. They all convert energy from ATP hydrolysis to exert mechanical stress upon interactions with microfilaments. Ongoing research is increasingly suggesting that at least seven kinds of myosins participate in the formation and development of cancer. Myosins play essential roles in cytokinesis failure, chromosomal and centrosomal amplification, multipolar spindle formation and DNA microsatellite instability. These are all prerequisites of tumor formation. Subsequently, myosins activate various processes of tumor invasion and metastasis development including cell migration, adhesion, protrusion formation, loss of cell polarity and suppression of apoptosis. In this review, we summarize the current understanding of the roles of myosins during tumorigenesis and discuss the factors and mechanisms which may regulate myosins in tumor progression. Furthermore, we put forward a completely new concept of “chromomyosin” to demonstrate the pivotal functions of myosins during karyokinesis and how this acts to optimize the functions of the members of the myosin superfamily.

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“…The majority of malignant solid tumours, including glioblastoma, show a hyperploid karyotype (Park et al . 1995).…”

Section: Discussionmentioning

confidence: 99%

Hyperploidy induced by drugs that inhibit formation of microtubule promotes chromosome instability

et al. 2002

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Background : Antimicrotubule drugs (AMDs), such as taxol and vincristine, are the most important addition to the chemotherapeutic armamentarium against human cancers. It has been shown that prolonged AMD treatment induces hyperploidy in G1-checkpoint-defective cancer cells and that these hyperploid cells subsequently undergo apoptosis. However, a fraction of these hyperploid cells are able to survive the prolonged mitotic stress and resume cell-cycle progression.

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Heterogeneity, polyploidy, aneusomy, and 9p deletion in human glioblastoma multiforme

Cited by 16 publications

References 45 publications

Deficiency in myosin light-chain phosphorylation causes cytokinesis failure and multipolarity in cancer cells

Deficiency in myosin light-chain phosphorylation causes cytokinesis failure and multipolarity in cancer cells

Myosins as fundamental components during tumorigenesis: diverse and indispensable

Hyperploidy induced by drugs that inhibit formation of microtubule promotes chromosome instability

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