| Summary: | To functionally analyze the role of AP-2γ as an ERα cofactor in breast cancer, we focused on
examining the phenotypic role of AP-2γ in breast cancer and question if AP-2γ is able to
reprogram the transcriptional network of ERα. From our knockdown experiments in MCF-7,
we had demonstrated that AP-2γ is not involved in cellular proliferation. Instead, it promotes
breast cancer by mediating cell survival. Furthermore, we showed that AP-2γ silencing
resulted in the down-regulation of ERα-upregulated genes, and this was verified by our over-
expression experiments in U2OS Tet-on-ERα, a cell line that lacks AP-2γ expression. Hence,
it can be ascertained that AP-2γ is required for the transcription of ERα-regulated genes.
However, we observed a minimal effect on promoting cell survival after over-expression of
AP-2γ in U2OS Tet-on-ERα. Such phenomenon could be explained by the requirement of
other transcription factors that might cooperate with AP-2γ in the reprogramming machinery.
Despite the partial reprogramming ability, we noticed a significant reduction in cell death in
EtOH-treated U2OS Tet-on-ERα. Therefore, we can suggest that AP-2γ is able to reprogram
the ERα transcription network to a certain extent.
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