Article Text

Download PDFPDF
B7-H4 Expression Promotes Tumorigenesis in Ovarian Cancer
  1. Lei Cheng*,
  2. Jie Jiang, MD, PhD*,
  3. Ran Gao,
  4. Shuangyan Wei,
  5. Fangfang Nan,
  6. Shaoru Li* and
  7. Beihua Kong*
  1. * Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan;
  2. Jining First People's Hospital, Jining; and
  3. Department of Obstetrics and Gynecology, the affiliated hospital of Binzhou University, Binzhou, Shandong, P.R. China.
  1. Address correspondence and reprint requests to Jie Jiang, MD, PhD, Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan 250012, Shandong Province, China. E-mail: jiangjie_jn{at}


Introduction: It has been previously shown that B7-H4, one of the B7 family members that serve as negative regulators of T cell function, has altered expression levels in a variety of cancers, overexpression of B7-H4 promotes cellular transformation. However, there is still lack of adequate evidence to establish a direct connection between B7-H4 expression and malignant transformation.

Methods: Herein, we constructed pE-green fluorescent protein-N1/B7-H4 mammalian expression vector and transfected into B7-H4-negative human ovarian cancer cell line SKOV3. Cellular proliferation, apoptosis, adhesion, motility, and invasion were examined in vitro. Cells injected subcutaneously into severe combined immunodeficient mouse were analyzed for the possible functions of B7-H4 in ovarian tumorigenesis in vivo.

Results: Fluorescence microscopy studies confirmed that the B7-H4-green fluorescent protein localizes in the cytoplasm of SKOV3/B7-H4 cells, whereas green fluorescent protein is uniformly distributed throughout the cell. B7-H4 promoted cellular proliferation rate and increased cell adhesion, migration, and invasion. In addition, SKOV3 cells expressing B7-H4 gained growth advantage in the xenograft model in vivo.

Conclusions: These studies demonstrate that B7-H4 directly promotes malignant transformation of ovarian cancer cell line, and provides a potential therapeutic strategy for targeting B7-H4 to inhibit progression of human ovarian cancers.

  • B7-H4
  • Ovarian cancer
  • Proliferation
  • Adhesion
  • Invasion

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.