EphA2 overexpression promotes ovarian cancer growth

Chunhua Lu, Mian M.K. Shahzad, Hua Wang, Charles N. Landen, Seung W. Kim, Julie Allen, Alpa M. Nick, Nicholas Jennings, Michael S. Kinch, Menashe Bar-Eli, Anil K. Sood

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


Background: Silencing EphA2 has been shown to result in anti-tumor efficacy. However, it is not known whether increasing EphA2 expression specifically results in increased tumor growth and progression. We examined the effects of stable EphA2 transfection into poorly invasive ovarian cancer cells with regard to in vitro invasive and in vivo metastatic potential. Results: In low cell density, EphA2-overexpressing A2780 cells (A2780-EphA2) displayed less cell-cell contact, increased cell-extracellular matrix (ECM) attachment and anchorage-independent cell growth compared to empty vector controls. There was no significant effect on anchorage-dependent cell proliferation, migration or invasion. Increased expression of EphA2 promoted tumor growth and enhanced the metastatic potential in A2780-EphA2 human ovarian cancer xenografts. The overexpression of EphA2 resulted in enhanced microvessel density (MVD), but had no effect on tumor cell proliferation. Methods: EphA2 gene was introduced into A2780 cells by retroviral infection. The effects of increased EphA2 expression were examined on cellular morphology, and anchorage-dependent and independent cell growth. Furthermore, the effect of EphA2 overexpression on metastatic ability was determined using an orthotopic nude mouse model of ovarian carcinoma. Conclusions: EphA2 promotes tumor growth by enhancing cell-ECM adhesion, increasing anchorage-independent growth and promoting angiogenesis.

Original languageEnglish
Pages (from-to)1098-1103
Number of pages6
JournalCancer Biology and Therapy
Issue number7
StatePublished - Jul 2008


  • EphA2
  • Ovarian cancer


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