PDCD2 functions in cancer cell proliferation and predicts relapsed leukemia

Nora Barboza, Svetlana Minakhina, Daniel J. Medina, Binaifer Balsara, Sonya Greenwood, Lien Huzzy, Arnold B. Rabson, Ruth Steward, Dale G. Schaar

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


PDCD2 is an evolutionarily conserved eukaryotic protein with unknown function. The Drosophlia pDCD2 ortholog Zfrp8 has an essential function in ly hematopoiesis. Zfrp8 mutants exhibit marked lymph gland hyperplasia that results from increased proliferation of partially diferentiated hemocytes, suggesting Zfrp8 may participate in cell growth. Based on the above observations we have focused on the role of pDCD2 in human cancer cell proliferation and hypothesized that aberrant pDCD2 expression may be characteristic of human malignancies. We report that pDCD2 is highly expressed in human acute leukemia cells as well as in normal hematopoietic progenitors. pDCD2 knockdown in cancer cells impairs their proliferation, but not viability relative to parental cells, supporting the notion that pDCD2 overexpression facilitates cancer cell growth. prospective analysis of pDCD2 in acute leukemia patients indicates pDCD2 RNa expression correlates with disease status and is a signiicant predictor of clinical relapse. pDCD2's role in cell proliferation and its high expression in human malignancies make it an attractive, novel potential molecular target for new anticancer therapies.

Original languageEnglish (US)
Pages (from-to)546-555
Number of pages10
JournalCancer Biology and Therapy
Issue number6
StatePublished - Jun 2013

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research


  • Acute lymphoblastic leukemia
  • Acute myelogenous leukemia
  • Cellular proliferation
  • Hematopoietic stem cells
  • PDCD2


Dive into the research topics of 'PDCD2 functions in cancer cell proliferation and predicts relapsed leukemia'. Together they form a unique fingerprint.

Cite this