In vitro study | The BCL6 inhibitor 79-6 has cell permeability and can selectively inhibit the transcriptional inhibition activity of BCL6, but does not affect the protein level of bcl6. 79-6 binds to an aromatic hydrocarbon pocket located in the lateral groove of the BTB region, inducing the destruction of the BCL6 transcriptional complex, reactivating the BCL6 target gene and selectively killing bcl6-dependent DLBCL cells. BCL6 interacts with MTA3 through the RD2 region, inhibiting terminal differentiation. BCL6 recruits CtBP through its DBD region, inhibiting its own activity. In MCF-7 and MDA231 cells, 79-6 inhibited cell invasion and colony formation, and enhanced E-cadherin mRNA expression by inhibiting bcl6. In breast cancer cells, 79-6 can reverse the function of BCL6 in the process of up-regulation of mesenchymal transition (EMT), cell invasion and E-cadherin transcriptional repression. |