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WT1/EGR1-mediated control of STIM1 expression and function in cancer cells Ritchie MF; Zhou Y; Soboloff JFront Biosci (Landmark Ed) 2011[Jun]; 16 (7): 2402-15There 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.|Brain Neoplasms/genetics/metabolism[MESH]|Breast Neoplasms/genetics/metabolism[MESH]|Calcium Signaling[MESH]|Early Growth Response Protein 1/genetics/*metabolism[MESH]|Female[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Genes, Tumor Suppressor[MESH]|Genes, Wilms Tumor[MESH]|Glioblastoma/genetics/metabolism[MESH]|Humans[MESH]|Leukemia, Myeloid, Acute/genetics/metabolism[MESH]|Male[MESH]|Membrane Proteins/genetics/*metabolism[MESH]|Models, Biological[MESH]|Neoplasm Proteins/genetics/*metabolism[MESH]|Neoplasms/genetics/*metabolism[MESH]|Oncogenes[MESH]|Ovarian Neoplasms/genetics/metabolism[MESH]|Prostatic Neoplasms/genetics/metabolism[MESH]|Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]|Stromal Interaction Molecule 1[MESH]|Transient Receptor Potential Channels/metabolism[MESH]|WT1 Proteins/*metabolism[MESH]|Wilms Tumor/genetics/metabolism[MESH] |
