Responses of normal and malignant cells to collagen, collagen-derived peptides and the C5-related tumor cell chemotactic peptide

Wass, John; Varani, James; Piontek, Gerald E.; Ward, Peter A.; Orr, F. W.

doi:10.1016/0045-6039(81)90024-5

Cited by 18 publications

(8 citation statements)

References 8 publications

(5 reference statements)

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“…It has been shown that collagen, a major component of most connective tissues (for review see Bornstein and Sage, 1980) and collagen-derived peptides are chemotactic for some tumor cells (Mundy et al, 1981). However, cells from a highly malignant fibrosarcoma cell line have been reported to lack chemotactic activity in response to collagen and collagen peptides, whereas cells from a nonmetastatic fibrosarcoma do respond as control cells (Wass et al, 1981). Cellular fibronectin, which is also present in connective tissues (for review see Hynes and Yamada, 1982) can therefore play a major role in recruitment of cells from certain tumors to connectivetissue-rich organs.…”

Section: Discussionmentioning

confidence: 99%

Enhanced chemotaxis of tumor‐derived and virus‐transformed cells to fibronectin and fibroblast‐conditioned medium

Mensing

Albini

Krieg

et al. 1984

Intl Journal of Cancer

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SV40 transformants of human embryo fibroblasts showed an enhanced chemotactic response to fibronectin and conditioned medium of fibroblasts in comparison to the non-transformed cells. An even higher chemotactic response was characteristic for a malignant human fibrosarcoma cell line, whereas cells derived from low-grade malignant dermatofibrosarcoma showed a normal response in the Boyden chamber assay. The high stimulation of chemotaxis is paralleled by a reduced synthesis and an altered deposition of fibronectin in the pericellular matrix of these cells. Both high chemotactic response and lack of deposition of fibronectin may play a role in tissue invasion and formation of metastasis by malignant tumors.

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Section: Discussionmentioning

confidence: 99%

Enhanced chemotaxis of tumor‐derived and virus‐transformed cells to fibronectin and fibroblast‐conditioned medium

Mensing

Albini

Krieg

et al. 1984

Intl Journal of Cancer

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“…The high malignant line responded to both of the chemotactic peptides and to TPA while the low malignant line was unresponsive. In this respect, the low This was not surprising because with regard to a number of other characteristics as well, the low malignant cells seem to be very similar to normal fibroblasts (17,24,(37)(38)(39). On the other hand, the rat peritoneal leukocytes and the two mylogenous cell lines did become hyperadherent when stimulated with TPA.…”

Section: Kinetics Of Stimulated Adherencementioning

confidence: 90%

“…Recent studies have shown that native collagen, intact ct collagen chains, and di and tri peptides derived from collagen are chemotactic for a variety of normal and malignant cell types. What is interesting is the fact that the spectrum of tumor cells which respond to the collagen peptides appears to be very similar to the spectrum of cells that respond to the bone factor (9,10,24). The nonmineral fraction of the bone matrix is, of course, nearly all collagen.…”

Section: Chemotactic Activation Of Tumor Cells In Vitromentioning

confidence: 99%

“…Among these are factors obtained from tumor tissue (4,5,22), a factor found in the supernatant fluids of bone cultures that have undergone metabolic resorption (9,23), lathyritic chick collagen, and collagen-derived peptides (10,24), a fragment obtained by limited proteolytic digestion of the C5a leukotactic peptide (8,25), and the synthetic trypeptide N-formyl-methionylleucyl-phenylalanine (FMLP) (16,17).…”

Section: Chemotactic Activation Of Tumor Cells In Vitromentioning

confidence: 99%

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Themotaxis of metastatic tumor cells

Varani

1982

Cancer Metast Rev

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A number of factors have been identified which are chemotactic for tumor cells. Recent studies have shown that, in addition to inducing directional motility in the Boyden chamber assay, these factors also induce a number of other responses. Included among these responses are cell swelling and foreign surface adhesiveness. The adherence response has been studied in detail using the Walker 256 carcinosarcoma cells and several other cell types. In the Walker cells, treatment with the C5a-derived tumor cell chemotactic peptide, the synthetic tripeptide, N-formyl-methionyl-leucyl-phenylalanine or with 12-O-tetradecanoyl phorbol ester induces a rapid, transient adherence response. The response is completely inhibited by several agents known to block the activity of phospholipase A2 or the metabolism of arachidonic acid through the lipoxygenase pathway but is not inhibited by inhibition of the cyclooxygenase pathway. This suggests that lipoxygenase metabolites of arachidonic acid may actually mediate the adherence response. It has been shown that chemotactic factor treatment of animals that are bearing circulating tumor cells induces a localization of these cells at the site of chemotactic factor injection. On the basis of these observations it has been hypothesized that tumor cells respond to chemotactic factors in much the same way that leukocytes do and that tumor cell localization at metastatic sites in vivo may be influenced by chemotactic factors in much the same way that leukocyte localization at inflammatory sites is.

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“…This is further supported by the observation that bone undergoing active resorption facilitated adhesion [12] and chemotaxis [13,14] of tumor cells to bone compared to non-resorbing bone. Collagen products appear to be one component of bone that induces tumor chemotaxis [15]. The factors through which bone induces chemotaxis are not clear.…”

Section: Chemotaxismentioning

confidence: 99%

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Keller

Zhang

Cooper

et al. 2001

Cancer and Metastasis Reviews

179

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The majority of men with progressive prostate cancer develop metastases with the skeleton being the most prevalent metastatic site. Unlike many other tumors that metastasize to bone and form osteolytic lesions, prostate carcinomas form osteoblastic lesions. However, histological evaluation of these lesions reveals the presence of underlying osteoclastic activity. These lesions are painful, resulting in diminished quality of life of the patient. There is emerging evidence that prostate carcinomas establish and thrive in the skeleton due to cross-talk between the bone microenvironment and tumor cells. Bone provides chemotactic factors, adhesion factors, and growth factors that allow the prostate carcinoma cells to target and proliferate in the skeleton. The prostate carcinoma cells reciprocate through production of osteoblastic and osteolytic factors that modulate bone remodeling. The prostate carcinoma-induced osteolysis promotes release of the many growth factors within the bone extracellular matrix thus further enhancing the progression of the metastases. This review focuses on the interaction between the bone and the prostate carcinoma cells that allow for development and progression of prostate carcinoma skeletal metastases.

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Responses of normal and malignant cells to collagen, collagen-derived peptides and the C5-related tumor cell chemotactic peptide

Cited by 18 publications

References 8 publications

Enhanced chemotaxis of tumor‐derived and virus‐transformed cells to fibronectin and fibroblast‐conditioned medium

Enhanced chemotaxis of tumor‐derived and virus‐transformed cells to fibronectin and fibroblast‐conditioned medium

Themotaxis of metastatic tumor cells

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