Open AccessRetracted: Blockade of ONECUT 2 expression in ovarian cancer inhibited tumor cell proliferation, migration, invasion and angiogenesis
Author(s) -
Lu Tongyi,
Wu Binhua,
Yu Yunfei,
Zhu Wenhui,
Zhang Simin,
Zhang Yinmei,
Guo Jiaying,
Deng Ning
Publication year - 2018
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.13633
Subject(s) - angiogenesis , cancer research , ovarian cancer , vascular endothelial growth factor a , cd31 , cell growth , biology , gene silencing , vascular endothelial growth factor , cancer , genetics , biochemistry , gene , vegf receptors
One cut homeobox 2 ( ONECUT 2 or OC ‐2) is a newly discovered transcription factor. Aberrant expression of OC ‐2 is closely related to cell proliferation, migration, invasion, and angiogenesis. In this study, we found that OC ‐2 expression was upregulated in ovarian adenocarcinoma cells, by Western blot analysis. The results of immunohistochemistry showed that the expression of OC ‐2 was also increased in malignant ovarian cancer tissue. In order to explore the role of OC ‐2 in the development of ovarian cancer, si RNA s that specifically targets OC ‐2 were designed. The si RNA targeting OC ‐2 could effectively inhibit the vascular endothelial growth factor A ( VEGFA ) expression, but silence and overexpression of VEGFA did not affect OC ‐2 expression. In addition, OC 2‐si RNA could block the proliferation, migration, and invasion, and inhibit epithelial–mesenchymal transition and the AKT / ERK signaling pathway, of human ovarian cancer cells in vitro. In a mouse model of ovarian cancer xenograft tumors, OC 2‐si RNA could significantly inhibit tumor cell growth and the tumor inhibition rate reached approximately 73%. The results of immunohistochemistry showed that the densities of microvessels stained with CD 31, the expression of OC ‐2 and VEGFA were significantly decreased in tumors. These data indicated that OC ‐2 was an upstream regulator of VEGFA and silencing OC ‐2 could inhibit ovarian cancer angiogenesis and tumor growth.