PURPOSE: ST7 has been proposed to be a tumor suppressor gene in the chromosome region 7q31.1-q31.2. In order to gain some insight into its role in cancer, the localization and verification of the ST7 expression levels were determined. METHODS: Various types of ST7 expression vectors tagged with the sequences of GFP, YFP or V5 were created using a gateway cloning system and full-length ST7 cDNA isolated from a human adult brain cDNA library. Cell cycle synchronization was also performed to analyze the expression of endogenous ST7 and its potentially related genes at each stage of the cell cycle. RESULTS: Cytosolic ST7 expression in HCT-116, MCF-7 and PC-3 cancer cell lines was detected via the fluorescence signal of the fusion proteins. ST7 translocation from the cytoplasm to the nucleus has not been observed in any of the conditions assayed. A cell cycle synchronization study demonstrated that both ST7 and SERPINE1 were overexpressed when cells were arrested. Expression of these genes was found to be diminished when the cells re-entered cell division status. In addition, we also found that Survivin, MMP-13 and Cyclin D1 were differentially expressed during the cell cycle. CONCLUSION: Our findings suggest that ST7 mediates tumor suppression through the regulation of the genes involved in maintaining the cellular structure of the cell and involved in oncogenic pathways.
PURPOSE: ST7 has been proposed to be a tumor suppressor gene in the chromosome region 7q31.1-q31.2. In order to gain some insight into its role in cancer, the localization and verification of the ST7 expression levels were determined. METHODS: Various types of ST7 expression vectors tagged with the sequences of GFP, YFP or V5 were created using a gateway cloning system and full-length ST7 cDNA isolated from a human adult brain cDNA library. Cell cycle synchronization was also performed to analyze the expression of endogenous ST7 and its potentially related genes at each stage of the cell cycle. RESULTS: Cytosolic ST7 expression in HCT-116, MCF-7 and PC-3 cancer cell lines was detected via the fluorescence signal of the fusion proteins. ST7 translocation from the cytoplasm to the nucleus has not been observed in any of the conditions assayed. A cell cycle synchronization study demonstrated that both ST7 and SERPINE1 were overexpressed when cells were arrested. Expression of these genes was found to be diminished when the cells re-entered cell division status. In addition, we also found that Survivin, MMP-13 and Cyclin D1 were differentially expressed during the cell cycle. CONCLUSION: Our findings suggest that ST7 mediates tumor suppression through the regulation of the genes involved in maintaining the cellular structure of the cell and involved in oncogenic pathways.
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