The ameboid motility of human and animal neoplastic cells

Enterline, Horatio T.; Coman, Dale Rex

doi:10.1002/1097-0142(1950)3:6<1033::aid-cncr2820030612>3.0.co;2-r

Cited by 70 publications

(24 citation statements)

References 16 publications

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“…In contrast to the mass movement of individual cells, cluster movement might serve to minimize cell loss from an initial population (i.e., solid tumor mass) and to decrease the possibility that dells might wander off in various directions. In vivo locomotion of entire tumor cell aggregates has been suggested for invasive V2 carcinoma (43,194). It has been demonstrated that small clusters of 3-5 V2 carcinoma cells sometimes move as units within the subcutaneous connective tissue.…”

Section: B Locomotionmentioning

confidence: 99%

Tumor invasion and host extracellular matrix

et al. 1983

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In this review some of the major mechanistic pathways by which tumor cells are thought to invade host tissues are discussed. Tumor invasion has been conceived to be the result of pathological, close-range interactions between malignant cells and host stroma. The sequence of events that characterize invasion can be summarized as follows: (a) Tumor cell clusters break from the confinement of the primary tumor. Loss of intercellular junctions (desmosomes), alterations in the chemical composition and physical properties of the cell surface coat (loss of fibronectin and heparan sulfate; excessive amounts of hyaluronate), and loosening of cell-substrate interactions (loss of hemidesmosomes, fibronectin, and heparan sulfate), are among the most frequently listed causes of tumor cell shedding. (b) Increased proteolytic activities at the invasion front cause focal alterations in the surrounding extracellular matrix, thereby changing its physical properties. Collagenases and cathepsins, as well as elastase and other neutral proteinases are the enzymes most frequently associated with matrix destruction and invasion. In some tissues this process is effectively regulated by inhibitors of matrix-degrading, proteolytic enzymes. (c) Tumor cells migrate into the altered matrix, possibly moving as aggregates along guidance tracks provided by host structures (blood vessels, lymphatics, nerves) or matrix macromolecules (collagen and fibronectin tracks). Migration seems to be preceded by increased swelling of glycosaminoglycan (i.e., hyaluronate) in the matrix, ahead of the migrating cell population. Various host cell types (mast cells, fibroblasts, endothelial cells, macrophages, etc.) may participate in these events.

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Section: B Locomotionmentioning

confidence: 99%

Tumor invasion and host extracellular matrix

et al. 1983

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“…It has been maintained, not without some cogency, that the following phenomena are responsible: (a) the mechanical pressure produced by the rapid proliferation of malignant tumors-force of tumor cells along tissue planes of least resistance; 1 (b) the attenuation in tumor cell adhesiveness-loss of the cell surface molecules cadherins and integrins; 2 (c) the increased tumor cell motility/amoeboid movements-secretion of motogenic cytokines such as the scatter factor/hepatocyte growth factor receptor (HGFR); [3][4][5][6][7][8] (d) the degradation of the extracellular matrix-release of several proteolytic enzymes, i.e., metalloproteases (stromelysin 3), collagenases, plasminogens, cathepsines; 5,9-11 (e) the stimulation of angiogenesis, through the secretion of vascular endothelial growth factor (VEGF) and thymidine phosphorylase (TP)-increased chances for malignant cells surviving and reaching the circulation. 12,13 Although the proposed mechanisms of cancer cell invasion are all valid, they must have been incomplete.…”

Section: Introductionmentioning

confidence: 99%

The pathology of tumor stromatogenesis

Giatromanolaki¹,

Sivridis²,

Koukourakis³

2007

Cancer Biology & Therapy

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Stromatogenesis is the formation of new, specific type, stroma at sites of active tumor cell invasion as an integral part of the invading process. The newly formed stroma by being wedged between tissue planes of least resistance disrupts the continuity of normal structures cleaving paths for the invading tumor cells-intramural stromatogenesis for endophytic tumors. Less frequently, the new stroma is formed towards a void space, i.e., at the free surfaces, whether internal or external (extramural stromatogenesis for exophytic tumors). It is postulated that the formation of this new stroma is generated and governed by the invading tumor cells with the tolerance and complicity of the adjacent activated fibroblasts. The spindle cells of the "neostroma" are intensely proliferating myofibroblasts, which are characterized by the frequent expression of a-smooth muscle actin and the particularly frequent expression of thymidine phosphorylase, PDGF-receptors and SPARC (secreted protein acidic rich in cysteine). The cellular and extracellular qualities, different as they are from those of reactive fibrosis, make stromatogenesis amenable to easy penetration by neoplastic cells and a prospective method for diagnosing early tumor invasion. Studies also suggest that the neostroma has complementary to cancer cell metabolic activity, important for buffering of cancer cell waste products and for the prevention of cancer cell acidic death. Thus, cancer cells and neostroma should not be seen as a mixture of heterogeneous uncoordinated cells but rather as a unified morphologic and metabolic domain with a harmonious collaboration between aerobic (myofibroblasts, endothelial cells) and anaerobic compartments (cancer cells).

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“…1. Full activity was found in a nonapeptide sequence, LB-3- (6)(7)(8)(9)(10)(11)(12)(13)(14), that includes one hydrophobic terminus-i.e., two leucines-and a terminus with the charged amino acid lysine. Thus, the presence of hydrophobicity at the carboxyl terminus and an amino acid with a side chain possessing a charge at the amino terminus is suggested as being significant for induction of cell spreading and motility inhibition in A375-M cells.…”

Section: Discussionmentioning

confidence: 99%

“…It is this latter property that most directly correlates with mortality (1)(2)(3)(4)(5)(6). To gain insight into the molecular mechanisms of metastasis, in vitro assays such as time-lapse video microscopy coupled with morphometric analyses have been developed; there appears to be a high correlation between motility of a cell type in culture and its metastatic behavior in vivo (7)(8)(9)(10)(11)(12).…”

mentioning

confidence: 99%

“…The latter activity has been localized to a 14-aminoacid sequence, residues 367-380 of the B chain of a-thrombin that includes loop "B" (residues 367-375) (13); the tetradecapeptide is designated LB-3- (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) herein. In the present work, the activity characteristics of this tetradecapeptide, which does not contain either thrombin's proteolytic activity or its mitogenic activity for fibroblasts, was assessed in cells belonging to a metastatic melanoma subclone (14); cell spreading was induced by a nanomolar peptide concentration.…”

mentioning

confidence: 99%

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Identification of a synthetic nonapeptide sequence that inhibits motility in culture of a melanoma subclone that possesses a high metastatic potential.

Packard

1987

Proc. Natl. Acad. Sci. U.S.A.

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A synthetic nonapeptide fragment of thrombin inhibits the cellular motility in culture of a human melanoma subclone that possesses a high metastatic potential in mice. Concomitant with the loss of ability to translocate in culture, these cells exhibit increases in the average length of actin cables and cellular surface area in contact with the substratum. The spreading activity is observed at a nonapeptide concentration of 1 nM within 1 hr of exposure at 370C. Pretreatment of cells with this nonapeptide does not block signal transduction through plasma membrane receptors for the following growth or differentiation factors: a-melanotropin (a-melanocyte-stimulating hormone), nerve growth factor, and transforming growth factor type (3. Results of the present study suggest an approach to cancer chemotherapy in which naturally occurring peptides from two functionally orthogonal classes may be used to perform two complementary functions: inhibition of metastasis and induction of differentiation.

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The ameboid motility of human and animal neoplastic cells

Cited by 70 publications

References 16 publications

Tumor invasion and host extracellular matrix

Tumor invasion and host extracellular matrix

The pathology of tumor stromatogenesis

Identification of a synthetic nonapeptide sequence that inhibits motility in culture of a melanoma subclone that possesses a high metastatic potential.

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