Open Access
Article
WT1/EGR1-mediated control of STIM1 expression and function in cancer cells
Michael F Ritchie1,Yandong Zhou1,Jonathan Soboloff1
1
Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
DOI: 10.2741/3862 Volume 16 Issue 7, pp.2402-2415
Published: 01 June 2011
Abstract

There have been numerous publications linking Ca(2+) signaling and cancer, however, a clear explanation for this link has remained elusive. We recently identified the oncogenes/tumor suppressors Wilms Tumor Suppressor 1 (WT1) and Early Growth Response 1 (EGR1) as regulators of the expression of STIM1, an essential regulator of Ca(2+) entry in non-excitable cells. The current review focuses on the literature defining both differential Ca(2+) signaling and WT1/EGR1 expression patterns in 6 specific cancer subtypes: Acute Myeloid Leukemia, Wilms Tumor, breast cancer, ovarian cancer, glioblastoma and prostate cancer. For each tumor-type, we have assessed how specific changes in WT1 and EGR1 expression might contribute to aberrant Ca(2+) homeostasis as well as the therapeutic potential of these observations.

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Michael F Ritchie, Yandong Zhou, Jonathan Soboloff. WT1/EGR1-mediated control of STIM1 expression and function in cancer cells. Frontiers in Bioscience-Landmark. 2011. 16(7); 2402-2415.