Authors:

Sarah Williams

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About Paper:

B-cell lymphoma X-large (BCL-XL) has been shown to promote breast cancer metastasis independently of its anti-apoptotic function. We designed 6 syngeneic mouse breast cancer models with genetic deletion of BCL-XL. Our preliminary tumor experiments showed opposing results with most models showing reduced metastasis by BCL-XL deletion and 1 model, Py8119, showing increased metastasis with BCL-XL deletion. We hypothesize that BCL-XL may play different roles in breast cancer metastasis depending on cellular cues from different cancer cells. We performed proteomic analysis on these cells lines to determine what molecular pathways were upregulated in the knockout (KO) lines that could contribute to this opposing phenotype in the Py8119 model. We found that there are multiple pathways contributing to metastasis, cell-cell junction, lipid metabolism, and kinase activity in the genetic KO line of Py8119 versus the wild-type (WT) line. We conclude that BCL-XL is a viable therapeutic target for treating breast cancer metastasis, but further investigation into cancer-specific BCL-XL targeting is needed. Our future efforts will focus on investigating why BCL-XL inhibits metastasis in some cancer models, which can be used as an exclusion criterion for BCL-XL-targeting therapy and potentially uncover a novel anti-tumorigenic role of BCL-XL in the tumor microenvironment. 497

Source:

University of Florida / 2024

Topics:

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Co-authors:

Sarah Williams