Autophagy is a lysosome-mediated catabolic process that is induced by cell stress and functions primarily in cell survival. Previous gene expression studies indicated that the transcription cofactor FHL2 is associated with both cell survival and autophagy in breast cancer cells, but the function of FHL2 in these processes was unknown. My hypothesis was that FHL2 is a component of the molecular machinery regulating survival and/or autophagy in breast cancer cells. To test this, FHL2 expression was examined in breast cancer cell lines following treatment with the autophagy-inducing breast cancer drugs, tamoxifen or epirubicin. These treatments resulted in no substantial change in levels of FHL2 transcripts or FHL2 protein. To assess FHL2 function, siRNA mediated knockdown and FHL2 over-expression approaches were employed in MCF7 breast cancer cells. FHL2 knockdown led to a significant decrease in cell viability, indicating that FHL2 may promote cell survival. Overexpression of FHL2 did not have a significant effect on viable cell numbers but resulted in increased levels of the autophagy protein LC3II, suggesting that elevated FHL2 may alter autophagy.
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Thesis advisor: Gorski, Sharon
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