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Submitted on March 29, 2005
Accepted on August 10, 2005
Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong; Departments of Physiology and PharmacologyThe University of Western Ontario, London, Ontario, Canada
Stanniocalcin-1 (STC1) is an endocrine hormone originally discovered in the corpuscles of Stannius (CS), endocrine glands on kidneys of bony fishes, and has also been identified in mammals. The mammalian STC1 gene is widely expressed in various tissues and appears to be involved in diverse biological processes. There is growing evidence to suggest that altered patterns of gene expression have a role in human cancer development. Recently, STC1 has been identified as a stimulator of mitochondrial respiration and has been hypothesized to be functionally related to the Warburg effect, of which HIF-1 plays a key role in reprogramming tumor metabolism. This prompted us to examine the involvement of HIF-1 in the regulation of STC1 expression in tumor hypoxia. Our data reveal that hypoxia can stimulate STC1 gene expression in various human cancer cell lines, including those derived from colon carcinomas (CaCo-2), nasopharyngeal cancer (CNE-2, HONE-1, HK-1) and ovarian cancer (CaOV3, OVCAR3, SKOV3). By far, the greatest response was observed in CNE-2 cells. In further studies on CNE-2 cells, desferrioxamine (DFX), cobalt chloride (CoCl2) and O2 depletion all increased HIF-1
protein and STC1 mRNA levels. DFX treatment, when coupled with Fe replenishment, abolished these effects. RNA interference studies further confirmed that endogenous HIF-1 was a key factor in hypoxia-induced STC1 expression. The ability of VEGF to stimulate STC1 expression in CNE-2 cells was comparatively low. Collectively, the present findings provide the first evidence of HIF-1 regulation of STC1 expression in human cancer cells. The studies have implications as to the role of STC1 in hypoxia induced adaptive responses in tumor cells.
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