Open AccessIn vivo delivery of si RNA targeting vasohibin‐2 decreases tumor angiogenesis and suppresses tumor growth in ovarian cancer
Author(s) -
Koyanagi Takahiro,
Suzuki Yasuhiro,
Saga Yasushi,
Machida Shizuo,
Takei Yuji,
Fujiwara Hiroyuki,
Suzuki Mitsuaki,
Sato Yasufumi
Publication year - 2013
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12297
Subject(s) - angiogenesis , ovarian cancer , cancer research , gene knockdown , in vivo , ovarian tumor , neovascularization , cell culture , chemistry , cancer , medicine , biology , microbiology and biotechnology , genetics
Vasohibin‐2 ( VASH 2) is a homolog of vasohibin‐1 and exhibits pro‐angiogenic activity. We recently reported that VASH 2 is expressed in certain ovarian cancers and promotes tumor growth through angiogenesis. To further demonstrate the effectiveness of molecular targeting of VASH 2 for anticancer treatment, we applied in vivo delivery of siRNA targeting VASH 2 (si VASH 2) using atelocollagen to a xenograft model of ovarian cancer. We inoculated mice s.c. with DISS and SKOV ‐3, two representative human ovarian serous adenocarcinoma cell lines. When tumors were measurable, we initiated treatment with control or si VASH 2 mixed with atelocollagen, which enveloped the whole tumor. Treatment with si VASH 2 significantly inhibited s.c. tumor growth by abrogating tumor angiogenesis. We confirmed that expression of VASH 2 mRNA in the tumor was downregulated by si VASH 2 treatment. In addition, the si VASH 2‐treated tumor contained more blood vessels covered with pericytes, indicating that knockdown of VASH 2 contributes to the normalization of tumor blood vessels. Based on these results, VASH 2 may be a promising molecular target for ovarian cancer treatment.