Turnover of Focal Adhesions and Cancer Cell Migration

Nagano, Makoto; Hoshino, Daisuke; Koshikawa, Naohiko; Akizawa, Toshifumi; Seiki, Motoharu

doi:10.1155/2012/310616

Cited by 214 publications

(205 citation statements)

References 93 publications

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“…However, it is noteworthy that an adoption of amoeboid-based migration for non-muscle cells was not always accompanied by an increase in migration speed. It was previously proposed that rapid movement based on bleb-based migration, was partly due to the simplicity of the focal adhesions between the cells and the matrix, with less time being needed to assemble and disassemble these structures [29]. However, our results show that blebbing does not always result in increased migration, possibly due to a mis-match in the molecules needed for effective focal adhesion formation.…”

Section: Discussioncontrasting

confidence: 57%

“…We suggest that non-muscle cells and satellite cells form different focal adhesions with the muscle fibre, possibly linked to their developmental history. The concept of developmental history regulating cell behaviour is well mapped in muscle, where it even segregates the properties of muscle stem cells [29]. Despite differing profiles of migration speeds, we show that the cell morphology adopted by non-muscle cells on fibres is regulated by the same molecular pathways.…”

Section: Discussionmentioning

confidence: 74%

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Mammalian Skeletal Muscle Fibres Promote Non-Muscle Stem Cells and Non-Stem Cells to Adopt Myogenic Characteristics

Morash

Collins‐Hooper

Mitchell

et al. 2017

Fibers

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Skeletal muscle fibres are unique cells in large animals, often composed of thousands of post-mitotic nuclei. Following skeletal muscle damage, resident stem cells, called satellite cells, commit to myogenic differentiation and migrate to carry out repair. Satellite stem cells migrate on muscle fibres through amoeboid movement, which relies on dynamic cell membrane extension and retraction (blebbing). It is not known whether blebbing is due to the intrinsic properties of satellite cells, or induced by features of the myofibre surface. Here, we determined the influence of the muscle fibre matrix on two important features of muscle regeneration: the ability to migrate and to differentiate down a myogenic lineage. We show that the muscle fibre is able to induce amoeboid movement in non-muscle stem cells and non-stem cells. Secondly, we show that prolonged co-culture on myofibres caused amniotic fluid stem cells and breast cancer cells to express MyoD, a key myogenic determinant. Finally, we show that amniotic fluid stem cells co-cultured on myofibres are able to fuse and make myotubes that express Myosin Heavy Chain.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 74%

Mammalian Skeletal Muscle Fibres Promote Non-Muscle Stem Cells and Non-Stem Cells to Adopt Myogenic Characteristics

Morash

Collins‐Hooper

Mitchell

et al. 2017

Fibers

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“…3A). In summary, expression of the metastasis suppressor, NDRG1, in both cell types decreases colocalization between p-paxillin and F-actin, which are involved in focal adhesion function, including tumor cell adhesion and migration (Nagano et al, 2012).…”

Section: And B)mentioning

confidence: 89%

Targeting the Metastasis Suppressor, N-Myc Downstream Regulated Gene-1, with Novel Di-2-Pyridylketone Thiosemicarbazones: Suppression of Tumor Cell Migration and Cell-Collagen Adhesion by Inhibiting Focal Adhesion Kinase/Paxillin Signaling

Wangpu

Lü

et al. 2016

Mol Pharmacol

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Metastasis is a complex process that is regulated by multiple signaling pathways, with the focal adhesion kinase (FAK)/ paxillin pathway playing a major role in the formation of focal adhesions and cell motility. N-myc downstream regulated gene-1 (NDRG1) is a potent metastasis suppressor in many solid tumor types, including prostate and colon cancer. Considering the antimetastatic effect of NDRG1 and the crucial involvement of the FAK/paxillin pathway in cellular migration and cell-matrix adhesion, we assessed the effects of NDRG1 on this important oncogenic pathway. In the present study, NDRG1 overexpression and silencing models of HT29 colon cancer and DU145 prostate cancer cells were used to examine the activation of FAK/paxillin signaling and the formation of focal adhesions. The expression of NDRG1 resulted in a marked and significant decrease in the activating phosphorylation of FAK and paxillin, whereas silencing of NDRG1 resulted in an opposite effect. The expression of NDRG1 also inhibited the formation of focal adhesions as well as cell migration and cell-collagen adhesion. Incubation of cells with novel thiosemicarbazones, namely di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone and di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone, that upregulate NDRG1 also resulted in decreased phosphorylation of FAK and paxillin. The ability of these thiosemicarbazones to inhibit cell migration and metastasis could be mediated, at least in part, through the FAK/paxillin pathway.

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“…Several studies reported a transport of integrins from the rear to the front of the cell during migration, maintaining the focal adhesion turnover. The presence of large focal adhesions creates more links to actin stress fibers and makes cell movement more difficult (110). The molecular structure of FAC includes integrins, intracellularly bound to paxillin and talin, which subsequently recruit FAK and vinculin.…”

Section: Actin Rearrangement Adhesion Complexes and Cellular Protrumentioning

confidence: 99%

Molecular Mechanisms of Glioma Cell Motility

et al. 2017

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Gliomas are the most common intracranial tumors in humans. The most malignant among these tumors is glioblastoma (GBM), with an incidence of 3-5 out of 100,000 persons in Western countries. GBM arises either de novo (primary GBM) or develops from a lower grade glioma (secondary GBM). The prognosis is poor. GBMs are lethal tumors and even optimal surgical resection, followed by chemotherapy and irradiation, results in a median survival of about 12-15 months. One characteristic that is responsible for GBM malignancy, and its worse prognosis, is the highly infiltrative growth of GBM cells into the healthy brain. GBM cell migration and invasion is a very complex process that is regulated by several factors, which include changes in the migrating cell itself as well as the tumor microenvironment. This chapter provides an overview of routes of invasion of glioma cells, the signaling pathways that drive glioma cell motility, and the processes through which glioma cells modulate their surrounding environment.

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Turnover of Focal Adhesions and Cancer Cell Migration

Cited by 214 publications

References 93 publications

Mammalian Skeletal Muscle Fibres Promote Non-Muscle Stem Cells and Non-Stem Cells to Adopt Myogenic Characteristics

Mammalian Skeletal Muscle Fibres Promote Non-Muscle Stem Cells and Non-Stem Cells to Adopt Myogenic Characteristics

Targeting the Metastasis Suppressor, N-Myc Downstream Regulated Gene-1, with Novel Di-2-Pyridylketone Thiosemicarbazones: Suppression of Tumor Cell Migration and Cell-Collagen Adhesion by Inhibiting Focal Adhesion Kinase/Paxillin Signaling

Molecular Mechanisms of Glioma Cell Motility

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