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Junco, V.

Publications and source records attributed to Junco, V..

2 recordsLinked to original sources

A novel interaction between MNT and CCDC6: structural insights and distinct roles in cell migration and the DNA damage response

MNT is a transcription factor of the MYC-MAX-MXD network whose biological functions remain incompletely understood. Here, we identify CCDC6, a tumor suppressor involved in the DNA damage response (DDR), as a novel MNT-interacting protein. Co-immunoprecipitation and interaction mapping analyses identified a part of the CCDC6 coiled-coil domain and the MNT bHLH-LZ region as major determinants of binding. Structural modelling further identified MNT residues predicted to mediate CCDC6 binding that are also critical for MNT-MAX dimerization. Transcriptomic analyses revealed substantial overlap between the gene expression programs regulated by MNT and CCDC6. Loss of either protein promoted cell migration, whereas MNT and CCDC6 cooperated in the regulation of {gamma}H2AX signalling, cisplatin responses and CCDC6 localization during the DDR. Together, our findings uncover a previously unrecognized connection between CCDC6 and the MYC-MAX-MXD network through its interaction with MNT, revealing an additional layer of regulation within this transcriptional network.

cancer biology↗

MYC directly transactivates CR2/CD21, the receptor of the Epstein-Barr virus, and enhances the viral infection of Burkitt lymphoma cells

The molecular hallmark of Burkitt lymphoma (BL) is a chromosomal translocation that results in deregulated expression of MYC oncogene. This translocation is present in virtually all BL. MYC is an oncogenic transcription factor deregulated in about half of total human tumors, by translocation or other mechanisms. Transcriptomic studies reveal more than 1000 genes regulated by MYC but a much smaller fraction of these genes is directly activated by MYC. All the endemic BL and many sporadic BL cells are associated to the Epstein-Barr virus (EBV) infection. The currently accepted mechanism for the MYC and BL association is that EBV is the causing agent inducing MYC translocation. Complement receptor 2 or CR2 (also called CD21) is a membrane protein that serves as EBV receptor in lymphoid cells. Here we show that CR2 is a direct MYC target gene. This conclusion is based on several evidences. First, MYC downregulation is linked to CR2 downregulation both in proliferating and in arrested cells. Second, MYC binds human CR2 promoter and this binding depends on E-box elements. Third, MYC activates CR2 promoter in an E-box dependent manner. Four, MYC activates CR2 transcription in the absence of protein synthesis. Importantly, MYC also induces CR2 expression in mouse primary B cells. Thus, CR2 is a bona fide MYC direct target gene. Moreover, higher MYC expression levels in Burkitt lymphoma-derived cells result in a more efficient EBV infection. We propose an alternative mechanism compatible with the correlation between EBV infection and MYC translocation observed in endemic BL, i.e., that deregulated MYC in BL cells occurs first and favors the EBV infection.

cancer biology↗