Classifying collective cancer cell invasion

Friedl, Peter; Locker, Joseph; Sahai, Erik; Segall, Jeffrey E.

doi:10.1038/ncb2548

Cited by 874 publications

(891 citation statements)

References 63 publications

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“…Tumor cells move either as individual cells or en masse via collective migration ( 27 ). Individual tumor cells have two different modes of movement: mesenchymal mode and amoeboid mode ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

et al. 2015

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We have recently identifi ed a metastasis suppressor gene for colorectal cancer: AES / Aes , which encodes an endogenous inhibitor of NOTCH signaling. When Aes is knocked out in the adenomatous epithelium of intestinal polyposis mice, their tumors become malignant, showing marked submucosal invasion and intravasation. Here, we show that one of the genes induced by NOTCH signaling in colorectal cancer is DAB1 / Dab1 . Genetic depletion of DAB1 suppresses cancer invasion and metastasis in the NOTCH signaling-activated mice. DAB1 is phosphorylated by ABL tyrosine kinase, which activates ABL reciprocally. Consistently, inhibition of ABL suppresses cancer invasion in mice. Furthermore, we show that one of the targets of ABL is the RAC/RHOGEF protein TRIO, and that phosphorylation at its Tyr residue 2681 (pY2681) causes RHO activation in colorectal cancer cells. Its unphosphorylatable mutation TRIO Y2681F reduces RHOGEF activity and inhibits invasion of colorectal cancer cells. Importantly, TRIO pY2681 correlates with signifi cantly poorer prognosis of patients with colorectal cancer after surgery. SIGNIFICANCE:These results indicate that TRIO pY2681 is one of the downstream effectors of NOTCH signaling activation in colorectal cancer, and can be a prognostic marker, helping to determine the therapeutic modality of patients with colorectal cancer. Cancer Discov; 5(2);[198][199][200][201][202][203][204][205][206][207][208][209][210][211]

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Section: Discussionmentioning

confidence: 99%

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

et al. 2015

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“…This is likely to be the result of an ATRA-dependent increase in intercellular contacts, as indicated by the relocaliza- tion of occludin to tight junctions (Fig. 6D), which causes a shift from single to collective cell migration (37).…”

Section: Cell Linementioning

confidence: 99%

“…To test whether these actions translate into inhibitory effects on the directional migration of SKBR3 cells, we used Boyden chambers. The studies were complemented by an analysis of the morphological traits of migrating cells performed with the use of wound assays (37). As expected, EGF and Herg caused a dramatic increase in SKBR3 cell migration (Fig.…”

Section: Cell Linementioning

confidence: 99%

All-trans-retinoic Acid Modulates the Plasticity and Inhibits the Motility of Breast Cancer Cells

Zanetti

Affatato

Centritto

et al. 2015

Journal of Biological Chemistry

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Background: All-trans-retinoic acid is a promising therapeutic agent in breast cancer. Results: All-trans-retinoic acid modulates mammary tumor cell epithelial-to-mesenchymal-transition via the TGF␤ and NOTCH pathways. Conclusion:The present study unveils a new aspect of all-trans-retinoic acid activity (i.e. regulation of phenotypic cell plasticity). Significance: Our results indicate that all-trans-retinoic acid is endowed with anti-metastatic properties that could be exploited at the therapeutic level.

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“…In breast cancer, it was determined that cancer cells signaled the secretion of chemokines by mesenchymal cells located in the stromal bed, and these chemokines stimulate cancer cells to become more aggressive and invasive. 35 Immune cells at tumor sites enable invasion by supplying MMPs. Tumor associated macrophages (TAMs) furnish cancer cells with growth factors and cancer cells reciprocate by providing colony stimulating factor 1 (CSF-1), thereby driving a more invasive behavior in tumor cells.…”

Section: Inflammation Induced Invasionmentioning

confidence: 99%

The role of endocytic Rab GTPases in regulation of growth factor signaling and the migration and invasion of tumor cells

Porther

Barbieri

2015

Small GTPases

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Metastasis is characterized pathologically by uncontrolled cell invasion, proliferation, migration and angiogenesis. It is a multistep process that encompasses the modulation of membrane permeability and invasion, cell spreading, cell migration and proliferation of the extracellular matrix, increase in cell adhesion molecules and interaction, decrease in cell attachment and induced survival signals and propagation of nutrient supplies (blood vessels). In cancer, a solid tumor cannot expand and spread without a series of synchronized events. Changes in cell adhesion receptor molecules (e.g., integrins, cadherin-catenins) and protease expressions have been linked to tumor invasion and metastasis. It has also been determined that ligand-growth factor receptor interactions have been associated with cancer development and metastasis via the endocytic pathway. Specifically, growth factors, which include IGF-1 and IGF-2 therapy, have been associated with most if not all of the features of metastasis. In this review, we will revisit some of the key findings on perhaps one of the most important hallmarks of cancer metastasis: cell migration and cell invasion and the role of the endocytic pathway in mediating this phenomenon

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Classifying collective cancer cell invasion

Cited by 874 publications

References 63 publications

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

Promotion of Colorectal Cancer Invasion and Metastasis through Activation of NOTCH–DAB1–ABL–RHOGEF Protein TRIO

All-trans-retinoic Acid Modulates the Plasticity and Inhibits the Motility of Breast Cancer Cells

The role of endocytic Rab GTPases in regulation of growth factor signaling and the migration and invasion of tumor cells

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