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[Cancer Research 28, 137-147, January 1, 1968]
© 1968 American Association for Cancer Research

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Phagocytosis and Degradation of Elastin by Normal and Tumor Cells in Culture1

Robert F. Gilfillan

Department of Pathology and Medical Research, St. Margaret's Hospital and Department of Obstetrics and Gynecology, Tufts University School of Medicine, Boston, Massachusetts 02125

Heteroploid, diploid, and primary kidney cells from several species have been examined in culture for their capacity to ingest and solubilize elastin, an important component of connective tissue.

Established human heteroploid cell lines and viral-transformed tumorigenic hamster cells actively phagocytized and degraded intracellular elastin. In contrast, established human diploid fibroblasts did not phagocytize elastin. Epithelial-like cellular elements of primary kidney cultures were less active phagocytically toward elastin than heteroploid cells and somewhat less active elastolytically. Fibroblast-like components of renal cultures, like human diploid fibroblasts, did not ingest fiber.

Uptake of elastin fiber by heteroploid cells could be essentially abolished by treatment with mild alkali, suggesting the removal of fiber-cell receptor substance.

Fiber ingestion and degradation of Hep-2 cells, accompanied by an increased metabolic activity, were modified by temperature, inhibitors of RNA and protein synthesis, and serum content. These findings suggest that phagocytosis of elastin is an active energy-requiring, receptor-dependent process.

Tumor and stromal cells in culture overlaid with elastin resemble to some degree host-tumor interface prior to invasion and destruction of blood vessel, tendon, and skin. These studies suggest that tumor and stromal cells provide models in which each cell type independently may be examined for its capacity to modify and catabolize fibrous components of connective tissue. Such models permit the characterization of these destructive events at the extracellular, the cellular, and the subcellular level.

1 Supported by Grant CA-08338, National Cancer Institute, NIH, USPHS.

Received 4/10/67. Accepted 9/27/67.




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[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1968 by the American Association for Cancer Research.