Elevated expression of CD93 promotes angiogenesis and tumor growth in nasopharyngeal carcinoma

Biochem Biophys Res Commun. 2016 Aug 5;476(4):467-474. doi: 10.1016/j.bbrc.2016.05.146. Epub 2016 May 30.

Abstract

CD93, also known as the complement component C1q receptor (C1qRp), has been reported to promote the progression of some cancer types. However, the expression and physiological significance of CD93 in nasopharyngeal carcinoma (NPC) remain largely elusive. In this study, we first examined the expression of CD93 in NPC and experimentally manipulated its expression. We observed that vascular CD93 expression is elevated in NPC and is correlated with T classification, N classification, distant metastasis, clinical stage and poor prognosis (all P < 0.05). In addition, overexpression of CD93 promoted angiogenesis in vitro. What's more, we found that CD93 was highly expressed in NPC tissues and cells, and the regulation of CD93 on cell proliferation was determined by cell counting kit (CCK)-8 assay and cell cycle analyses. Our findings provide unique insight into the pathogenesis of NPC and underscore the need to explore novel therapeutic targets such as CD93 to improve NPC treatment.

Keywords: Angiogenesis; CD93; Nasopharyngeal carcinoma (NPC); Proliferation.

MeSH terms

  • Carcinoma
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Gene Expression
  • Gene Knockdown Techniques
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Immunohistochemistry
  • Male
  • Membrane Glycoproteins / antagonists & inhibitors
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Middle Aged
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / blood supply*
  • Nasopharyngeal Neoplasms / immunology*
  • Nasopharyngeal Neoplasms / pathology
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / immunology
  • RNA, Small Interfering / genetics
  • Receptors, Complement / antagonists & inhibitors
  • Receptors, Complement / genetics
  • Receptors, Complement / metabolism*

Substances

  • Membrane Glycoproteins
  • RNA, Small Interfering
  • Receptors, Complement
  • complement 1q receptor