TY - JOUR
T1 - An invasion-independent pathway of blood-borne metastasis
T2 - A new murine mammary tumor model
AU - Sugino, Takashi
AU - Kusakabe, Takashi
AU - Hoshi, Nobuo
AU - Yamaguchi, Tomiko
AU - Kawaguchi, Takanori
AU - Goodison, Steve
AU - Sekimata, Masayuki
AU - Homma, Yoshimi
AU - Suzuki, Toshimitsu
N1 - Funding Information:
Supported by a Grant-in-Aid for Scientific Research (C) (no. 12670212) from the Ministry of Education, Science, Sports, and Culture, Japan.
PY - 2002
Y1 - 2002
N2 - It is generally believed that active invasion by cancer cells is essential to the metastatic process. In this report, we describe a murine mammary tumor (MCH66) model of metastasis that does not require invasion into the vascular wall of both the primary tumor and the target organ, in this case, the lung. The process involves intravasation of tumor nests surrounded by sinusoidal blood vessels, followed by intravascular tumor growth in the lung, without penetration of the vascular wall during the process. Comparative studies using a non-metastatic MCH66 clone (MCH66C8) and another highly invasive metastatic cell line (MCH416) suggested that high angiogenic activity and sinusoidal remodeling of tumor blood vessels were prerequisites for MCH66 metastasis. Differential cDNA analysis identified several genes that were overexpressed by MCH66, including genes for the angiogenesis factor pleiotrophin, and extracellular matrix-associated molecules that may modulate the microenvironment toward neovascularization. Our analyses suggest that tumor angiogenesis plays a role in the induction of invasion-independent metastasis. This model should prove useful in screening and development of new therapeutic agents for cancer metastasis.
AB - It is generally believed that active invasion by cancer cells is essential to the metastatic process. In this report, we describe a murine mammary tumor (MCH66) model of metastasis that does not require invasion into the vascular wall of both the primary tumor and the target organ, in this case, the lung. The process involves intravasation of tumor nests surrounded by sinusoidal blood vessels, followed by intravascular tumor growth in the lung, without penetration of the vascular wall during the process. Comparative studies using a non-metastatic MCH66 clone (MCH66C8) and another highly invasive metastatic cell line (MCH416) suggested that high angiogenic activity and sinusoidal remodeling of tumor blood vessels were prerequisites for MCH66 metastasis. Differential cDNA analysis identified several genes that were overexpressed by MCH66, including genes for the angiogenesis factor pleiotrophin, and extracellular matrix-associated molecules that may modulate the microenvironment toward neovascularization. Our analyses suggest that tumor angiogenesis plays a role in the induction of invasion-independent metastasis. This model should prove useful in screening and development of new therapeutic agents for cancer metastasis.
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U2 - 10.1016/S0002-9440(10)61147-9
DO - 10.1016/S0002-9440(10)61147-9
M3 - Article
C2 - 12057902
AN - SCOPUS:0036087843
SN - 0002-9440
VL - 160
SP - 1973
EP - 1980
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 6
ER -