Regulation of cancer cell motility through actin reorganization

Yamazaki, Daisuke; Kurisu, Shusaku; Takenawa, Tadaomi

doi:10.1111/j.1349-7006.2005.00062.x

Cited by 544 publications

(500 citation statements)

References 53 publications

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“…Differences between control and MCF-7/AZ.Pcad cells were evident as P-cadherin-overexpressing cells showed an increase in membrane ruffling and in actin cellular extensions, as well as in their cytoplasmic area ( Figure 5). Indeed, P-cadherinoverexpressing cells, including MCF-7/AZ.Pcad and BT-20, show an upper cell localized nuclei and appear as rounded and flat cells with actin-rich sheet-like membrane protrusive structures that, according with the literature, are essentially observed during crawling cell motility and spreading (Yamazaki et al, 2005;Chhabra and Higgs, 2007). Using double F-actin and p120ctn staining, MCF-7/AZ.Mock versus MCF-7/AZ.Pcad cells showed distinct aggregation ability, where MCF-7/AZ.Mock cells, in contrast to P-cadherin-overexpressing cells, showed well-formed and tight aggregates ( Figure 5).…”

Section: Soluble P-cadherin Induces Breast Cancer Cell Invasionsupporting

confidence: 52%

“…Indeed, microscopic fluorescence imaging of P-cadherin expressing cells showed that P-cadherin destabilizes cell-cell adhesion, promoting cytoskeleton changes, leading to a different cell phenotype. The cells resemble the aggressive morphology observed in primary basallike P-cadherin-positive breast carcinomas, as these cells normally acquire a large cytoplasm and several membrane protrusions, and cell-cell adhesion is not usually mediated by a compact zipper-like structure (Yamazaki et al, 2005;Chhabra and Higgs, 2007).…”

Section: Soluble P-cadherin Induces Breast Cancer Cell Invasionmentioning

confidence: 73%

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Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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Cell-cell adhesion is an elementary process in normal epithelial cellular architecture. Several studies have shown the role mediated by cadherins in this process, besides their role in the maintenance of cell polarity, differentiation and cell growth. However, during tumour progression, these molecules are frequently altered. In breast cancer, tumours that overexpress P-cadherin usually present a high histological grade, show decreased cell polarity and are associated with worse patient survival. However, little is known about how this protein dictates the very aggressive behaviour of these tumours. To achieve this goal, we set up two breast cancer cell models, where P-cadherin expression was differently modulated and analysed in terms of cell invasion, motility and migration. We show that P-cadherin overexpression, in breast cancer cells with wild-type E-cadherin, promotes cell invasion, motility and migration. Moreover, we found that the overexpression of P-cadherin induces the secretion of matrix metalloproteases, specifically MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage. Further, we showed that soluble P-cadherin fragment is able to induce in vitro invasion of breast cancer cells. Overall, our results contribute to elucidate the mechanism underlying the invasive behaviour of P-cadherin expressing breast tumours.

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Section: Soluble P-cadherin Induces Breast Cancer Cell Invasionsupporting

confidence: 52%

Section: Soluble P-cadherin Induces Breast Cancer Cell Invasionmentioning

confidence: 73%

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

et al. 2009

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“…Thus, it is possible that not only integrin β1, but also MT1-MMP is activated by irradiation, resulting in increased migration of IR cells. Furthermore, the formation of membrane protrusions at the leading edge of migrating cells, as a result of actin reorganization, is regulated by one of the small GTPases, Rac [12], and activated Rac1 induces integrin-dependent migration in mammary epithelial cells [13]. Therefore, Rac activity might be necessary to induce invasiveness in IR cells.…”

Section: Discussionmentioning

confidence: 99%

Integrin β1-dependent invasive migration of irradiation-tolerant human lung adenocarcinoma cells in 3D collagen matrix

Ishihara

Haga

Yasuda

et al. 2010

Biochemical and Biophysical Research Communications

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Radiotherapy is one of the effective therapies used for treating various malignant tumors.However, the emergence of tolerant cells after irradiation remains problematic due to their high metastatic ability, sometimes indicative of poor prognosis. In this study, we showed that subcloned human lung adenocarcinoma cells (A549P-3) that are irradiation-tolerant indicate high invasive activity in vitro, and exhibit an integrin β1 activity-dependent migratory pattern.In collagen gel overlay assay, majority of the A549P-3 cells displayed round morphology and low migration activity, whereas a considerable number of A549P-3IR cells surviving irradiation displayed a spindle morphology and high migration rate. Blocking integrin β1 activity reduced the migration rate of A549P-3IR cells and altered the cell morphology allowing them to assume a round shape. These results suggest that the A549P-3 cells surviving irradiation acquire a highly invasive integrin β1-dependent phenotype, and integrin β1 might be a potentially effective therapeutic target in combination with radiotherapy.

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“…Cell migration is a critical step for metastasis, and thus control of cell migration via the actin cytoskeleton provides the possibility for regulation of metastasis [38]. We identified 9 up-regulated and 19 downregulated genes with cytoskeleton-related functions.…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

et al. 2006

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SummaryRenal cell carcinoma (RCC) is the most common malignancy in adult kidney, and accounts for 3% of malignancies worldwide with increasing incidence. Clear cell RCC (ccRCC) is the major type in RCC. Resection by surgery is the main treatment because the response of ccRCC to traditional therapies is very poor. To identify the tumor-associated genes for better understanding the molecular mechanism of ccRCC, the full-length enriched cDNA libraries of ccRCC and normal kidney tissues were constructed by the oligo-capping method. Nucleotide sequences of the cDNA libraries of ccRCC and normal kidney tissues were sequenced. From the sequence analysis of 19,425 and 12,400 clones of ccRCC and normal kidney tissues, 4356 and 3055 genes were identified, respectively. By comparing the gene-expression patterns of ccRCC and normal tissues, the up-or down-regulated genes were identified. Among these identified genes, the differential expression of annexin A2 and argininosuccinate synthetase genes were further confirmed by quantitative real-time PCR and Western blot analysis.

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Regulation of cancer cell motility through actin reorganization

Cited by 544 publications

References 53 publications

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Extracellular cleavage and shedding of P-cadherin: a mechanism underlying the invasive behaviour of breast cancer cells

Integrin β1-dependent invasive migration of irradiation-tolerant human lung adenocarcinoma cells in 3D collagen matrix

Identification of differentially expressed genes in clear cell renal cell carcinoma by analysis of full-length enriched cDNA library

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