Ascites Form of a Human Cancer Serially Transplantable in Nude Mice

1976 ◽  
Vol 57 (4) ◽  
pp. 965-967 ◽  
Author(s):  
Voshito Ueyama ◽  
Vukio Kondo ◽  
Norikazu Tamaoki ◽  
Nakaaki Ohsawa
Keyword(s):  
1996 ◽  
Vol 38 (0) ◽  
pp. S48-S52 ◽  
Author(s):  
Naoko Kajimura ◽  
Hideaki Iseki ◽  
R. Tanaka ◽  
Chiharu Ohue ◽  
Kotomi Otsubo ◽  
...  

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2305 ◽  
Author(s):  
Yu-Cheng Chou ◽  
Meng-Ya Chang ◽  
Hsu-Tung Lee ◽  
Chiung-Chyi Shen ◽  
Tomor Harnod ◽  
...  

Phenethyl isothiocyanate (PEITC) from cruciferous vegetables can inhibit the growth of various human cancer cells. In previous studies, we determined that PEITC inhibited the in vitro growth of human glioblastoma GBM 8401 cells by inducing apoptosis, inhibiting migration and invasion, and altering gene expression. Nevertheless, there are no further in vivo reports disclosing whether PEITC can suppress the growth of glioblastoma. Therefore, in this study we investigate the anti-tumor effects of PEITC in a xenograft model of glioblastoma in nude mice. Thirty nude mice were inoculated subcutaneously with GBM 8401 cells. Mice with one palpable tumor were divided randomly into three groups: control, PEITC-10, and PEITC-20 groups treated with 0.1% dimethyl sulfoxide (DMSO), and 10 and 20 μmole PEITC/100 μL PBS daily by oral gavage, respectively. PEITC significantly decreased tumor weights and volumes of GBM 8401 cells in mice, but did not affect the total body weights of mice. PEITC diminished the levels of anti-apoptotic proteins MCL-1 (myeloid cell leukemia 1) and XIAP (X-linked inhibitor of apoptosis protein) in GBM 8401 cells. PEITC enhanced the levels of caspase-3 and Bax in GBM 8401 cells. The growth of glioblastoma can be suppressed by the biological properties of PEITC in vivo. These effects might support further investigations into the potential use of PEITC as an anticancer drug for glioblastoma.


2018 ◽  
Author(s):  
Friederike I. Nollmann ◽  
Patricia Perez Galan ◽  
Javier Garcia Fernandez ◽  
Heidi K. Walter ◽  
Johannes P. Magnusson ◽  
...  

1999 ◽  
Vol 44 (3) ◽  
pp. 177-186 ◽  
Author(s):  
Vernon Knight ◽  
Nadezhda V. Koshkina ◽  
J. Clifford Waldrep ◽  
Beppino C. Giovanella ◽  
Brain E. Gilbert
Keyword(s):  

1992 ◽  
Vol 4 (4) ◽  
pp. 30-32
Author(s):  
Binxue Zhang ◽  
Yao Tang ◽  
Jie Zheng ◽  
Cheng Yin ◽  
Jieliang Wang ◽  
...  

1978 ◽  
Vol 60 (4) ◽  
pp. 925-929 ◽  
Author(s):  
Seiichi Takahashi ◽  
Yoichi Konishi ◽  
Katsunori Nakatani ◽  
Shoji Inui ◽  
Kiyohide Kojima ◽  
...  

2004 ◽  
Vol 15 (4) ◽  
pp. 1600-1608 ◽  
Author(s):  
Nina Wittenmayer ◽  
Burkhard Jandrig ◽  
Martin Rothkegel ◽  
Kathrin Schlüter ◽  
Wolfgang Arnold ◽  
...  

Profilin 1 (PFN1) is a regulator of the microfilament system and is involved in various signaling pathways. It interacts with many cytoplasmic and nuclear ligands. The importance of PFN1 for human tissue differentiation has been demonstrated by the findings that human cancer cells, expressing conspicuously low PFN1 levels, adopt a nontumorigenic phenotype upon raising their PFN1 level. In the present study, we characterize the ligand binding site crucial for profilin's tumor suppressor activity. Starting with CAL51, a human breast cancer cell line highly tumorigenic in nude mice, we established stable clones that express PFN1 mutants differentially defective in ligand binding. Clones expressing PFN1 mutants with reduced binding to either poly-proline-stretch ligands or phosphatidyl-inositol-4,5-bisphosphate, but with a functional actin binding site, were normal in growth, adhesion, and anchorage dependence, with only a weak tendency to elicit tumors in nude mice, similar to controls expressing wild-type PFN1. In contrast, clones expressing a mutant with severely reduced capacity to bind actin still behaved like the parental CAL51 and were highly tumorigenic. We conclude that the actin binding site on profilin is instrumental for normal differentiation of human epithelia and the tumor suppressor function of PFN1.


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