Tid1 modulation of p53 ubiquitination in breast cancer cells

Date
2012
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Abstract
In this study, we showed that Tumorous Imaginal Disc 1 (Tidl) has the ability to indirectly modulate p53 ubiquitination in breast cancer cells. The over-expression of Tidl expression in MCF-7 cells led to suppression of p53 ubiquitination whereas its suppression led to enhanced ubiquitination. Tid 1 mediated suppression of p53 ubiquitination can enhance p53 half-life but not endogenous p53 level or p53 downstream targets. Over-expression of Tidl alone was unable to decrease the cell viability of MCF-7 cells but its combination with the proteasome inhibitor ALLN, there was a decrease in cell viability. A reduction in ATP level by Tidl over-expression is suggested to be one of the possible mechanisms that may suppress p53 ubiqutination. In summary, we propose that Tid 1 depletes cellular ATP levels, which in tum, inhibits ubiquitination­proteasome machinery, resulting in enhanced stability of p53.
Description
Bibliography: p. 89-103
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Citation
Kim, S. H. (2012). Tid1 modulation of p53 ubiquitination in breast cancer cells (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/4942
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