Enhanced metastatic potential of cloned low-metastatic Lewis lung carcinoma cells treated in vitro with dimethyl sulfoxide.

نویسنده

  • K Takenaga
چکیده

Treatment of low-metastatic Lewis lung carcinoma cells (P-29) with dimethyl sulfoxide in vitro enhanced their lung-colonizing ability. The concentration of dimethyl sulfoxide used delayed the in vitro growth of P-29 cells but was not cytotoxic. The arrest and retention in the lung of untreated and dimethyl sulfoxide-treated P-29 cells labeled with 5-[125I]iodo-2'-deoxyuridine after injecting them into a tail vein of syngeneic mice were examined. Dimethyl sulfoxide-treated P-29 cells were trapped in the lung more than untreated cells and were cleared from the lungs more slowly than untreated cells. Treatment of P-29 cells with dimethyl sulfoxide resulted in the increase in their homotypic aggregation and adhesion to plastic culture dishes, monolayers of endothelial cells, and a subendothelial extracellular matrix. This treatment also increased significantly their activities of degradative enzymes, such as glycosidases and cathepsin B, and their production of plasminogen activator. These results indicate that the enhanced lung-colonizing ability of P-29 cells treated with dimethyl sulfoxide is due to the increase in adhesiveness, resulting in arrest and retention of the cells in the lung of the host and in the increase in their degradative enzyme activities. The enhancing effect of dimethyl sulfoxide on the lung-colonizing ability of P-29 cells was found to be reversible.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Metastatic heterogeneity of cells from Lewis lung carcinoma.

To allow investigations of the role of tumor cell proteases in invasion and metastasis, an attempt was made to obtain well-defined homogeneous populations of Lewis Lung carcinoma cells differing widely in their metastatic potential. From a single Lewis lung carcinoma, a parental line of cells was established and subsequently cloned so as to provide 18 clonal tumor cell lines. These clones diffe...

متن کامل

Effect of prostaglandin E2-producing nonmetastatic Lewis lung carcinoma cells on the migration of prostaglandin E2-responsive metastatic Lewis lung carcinoma cells.

The role of prostaglandin E2 (PGE2) in directly stimulating metastatic spread by Lewis lung carcinoma (LLC) cells was examined with the use of an in vitro migration model for tumor dissemination. The extent to which cloned metastatic and nonmetastatic LLC cells migrated out of glass capillary tubes in vitro reflected their capacity to form pulmonary metastases in vivo. The addition of PGE2 to m...

متن کامل

Loss of tumorigenicity of Lewis lung carcinoma on the chorioallantoic membrane of the chick embryo.

The Lewis lung carcinoma is a transplantable metastatic tumor of the C57BL mouse strain. When cells derived from this tumor are inoculated onto the chorioallantoic membrane (CAM) of 9- to 11-day-old chick embryos, large tumors are produced. Although most of these tumors contain mouse cells, they can no longer be transplanted either in C57BL mice or on the CAM. Cloned cells obtained from Lewis l...

متن کامل

Loss of Tumorigenicity of Lewis Lung Carcinoma on the Chorioallantoic Membrane of the Chick Embryo1

The Lewis lung carcinoma is a transplantable metastatic tumor of the C57BL mouse strain. When cells derived from this tumor are inoculated onto the Chorioallantoic membrane (CAM) of 9to 11-day-old chick embryos, large tumors are produced. Although most of these tumors contain mouse cells, they can no longer be transplanted either in C57BL mice or on the CAM. Cloned cells obtained from Lewis lun...

متن کامل

Cytochalasin D promotes pulmonary metastasis of B16 melanoma through expression of tissue factor.

Cytochalasin D (CytD) targets actin, a ubiquitous protein in eukaryotic cells. Previous studies have focused mainly on the antitumor effects of CytD. We previously found CytD to promote lung metastasis in B16 melanoma cells, which we had not anticipated, and, therefore, in the present study we investigated the possible underlying mechanisms. B16 melanoma cells were co-cultured with CytD and oth...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cancer research

دوره 44 3  شماره 

صفحات  -

تاریخ انتشار 1984