Relationships between morphology, dissemination, migration, and prostaglandin E2 secretion by cloned variants of Lewis lung carcinoma.

Lewis lung carcinoma cells (LLC) were isolated and cloned from metastatic lung nodules of C57BL/6 mice or from a cultured parental LLC line. Their dissemination abilities were defined in vivo by their capacities to disseminate to the lungs following s.c. or i.v. injection into mice and in an in vitro model for tumor dissemination by their ability to migrate out of glass capillary tubes. Cloned LLC cells with an enhanced dissemination capacity exhibited a rounded morphology, were nonadherent during in vitro culture, and readily migrated out of capillary tubes. In contrast, clones not capable of dissemination were adherent and spread during in vitro culture and did not migrate out of capillary tubes. Production of prostaglandin E2 by these clones was measured by a radioimmunoassay. An inverse relationship was observed between the extent of migration and dissemination of clones and their ability to secrete prostaglandin E2 in vitro and in vivo. However, the prostaglandin E2 did not regulate the migration-dissemination capacities of LLC clones as inhibiting prostaglandin synthesis did not alter their capacity to migrate in vitro or to lodge in the lungs following i.v. inoculation into mice.

[1]  B. Zetter,et al.  Organ-specific adhesion of metastatic tumor cells in vitro. , 1984, Science.

[2]  M. Young,et al.  Prostaglandin E production by Lewis lung carcinoma: mechanism for tumor establishment in vivo. , 1984, Journal of the National Cancer Institute.

[3]  A. Fulton Effects of indomethacin on the growth of cultured mammary tumors , 1984, International journal of cancer.

[4]  A. van Lamsweerde,et al.  Metastatic heterogeneity of cells from Lewis lung carcinoma. , 1983, Cancer research.

[5]  C. Ting,et al.  Activation of natural killer-derived cytotoxic T lymphocytes. I. Regulation by macrophage and prostaglandins. , 1983, Journal of immunology.

[6]  A. Ben-Ze'ev,et al.  Modulation of the metastatic capability in B16 melanoma by cell shape. , 1983, Science.

[7]  M. Young,et al.  Enhancement of immune function and tumor growth inhibition by antibodies against prostaglandin E2. , 1983, Immunological communications.

[8]  G Poste,et al.  Evolution of tumor cell heterogeneity during progressive growth of individual lung metastases. , 1982, Proceedings of the National Academy of Sciences of the United States of America.

[9]  G. Nicolson,et al.  Tumor metastasis is not due to adaptation of cells to a new organ environment. , 1982, Science.

[10]  J. Bertram,et al.  Inhibition of growth of primary and metastatic Lewis lung carcinoma cells by the phosphodiesterase inhibitor isobutylmethylxanthine. , 1980, Cancer research.

[11]  P. Ward,et al.  Adhesive characteristics of tumor cell variants of high and low tumorigenic potential. , 1980, Journal of the National Cancer Institute.

[12]  P. Ward,et al.  Hydrolytic enzyme activities, migratory activity, and in vivo growth and metastatic potential of recent tumor isolates. , 1979, Cancer research.

[13]  F. Fitzpatrick,et al.  Prostaglandin D2 formation by malignant melanoma cells correlates inversely with cellular metastatic potential. , 1979, Proceedings of the National Academy of Sciences of the United States of America.

[14]  G. Sundharadas,et al.  Characteristics of a low‐molecular‐weight factor extracted from mouse tumors that affects in vitro properties of macrophages , 1979, International journal of cancer.

[15]  I. Fidler,et al.  Metastatic heterogeneity of cells from an ultraviolet light-induced murine fibrosarcoma of recent origin. , 1978, Cancer research.

[16]  I. Pastan,et al.  Cellular transformation and the ‘morphologic phenotype’ of transformed cells , 1978, Nature.

[17]  G. Nicolson,et al.  Tumor cell and host properties affecting the implantation and survival of blood-borne metastatic variants of B16 melanoma. , 1978, Israel journal of medical sciences.

[18]  T. Żebro,et al.  Prostaglandins from tumours of human large bowel. , 1977, British Journal of Cancer.