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Mouse Colon Carcinoma Cells Established for High Incidence of Experimental Hepatic Metastasis Exhibit Accelerated and Anchorage-Independent Growth
Authors:Megumi?Morimoto-Tomita,Yoshimi?Ohashi,Azusa?Matsubara,Makoto?Tsuiji,Tatsuro?Irimura  author-information"  >  author-information__contact u-icon-before"  >  mailto:irimura@mol.f.u-tokyo.ac.jp"   title="  irimura@mol.f.u-tokyo.ac.jp"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:(1) Laboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan;(2) Department of Anatomy, University of California, San Francisco, California, USA;(3) Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo,Bunkyo-ku, Tokyo 113-0033, Japan
Abstract:Highly metastatic variants of mouse colon 38 colon carcinoma cells were established by repeated selection in vivo for liver metastasis and designated as SL4 cells. The SL4 cells formed colonies in the liver of 100% of syngenic mice when injected intrasplenically, while the incidence of liver metastasis was 27% of mice injected with parental cells. The weight of livers, which is an indicator of experimental hepatic metastasis formation, was significantly higher after intrasplenic injection and subsequent splenoctomy with SL4 cells than colon 38 cells. The incidence of hepatic metastasis after intracecal injection of SL4 cells was significantly higher than that of colon 38 cells. The SL4 cells were tested in vitro for their properties. Differences were not detected in the motility and invasive behavior between colon 38 cells and SL4 cells. SL4 cells showed a higher proliferation rate than colon 38 cells under adherent conditions. SL4 cells maintained a capacity to proliferate under non-adherent conditions whereas parental cells did not. SL4 cells should be a useful tool to study the mechanism of hepatic metastasis of colon carcinoma cells and to develop methods to prevent hepatic metastasis.
Keywords:anchorage-independent growth  cell cycle  colon carcinoma  liver metastasis
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