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  1. Article ; Online: Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation.

    Jones, Cheyenne A / Tansey, William P / Weissmiller, April M

    Epigenetics insights

    2022  Volume 15, Page(s) 25168657221115656

    Abstract: The SWI/SNF chromatin remodeling complex uses the energy of ATP hydrolysis to alter contacts between DNA and nucleosomes, allowing regions of the genome to become accessible for biological processes such as transcription. The SWI/SNF chromatin remodeler ... ...

    Abstract The SWI/SNF chromatin remodeling complex uses the energy of ATP hydrolysis to alter contacts between DNA and nucleosomes, allowing regions of the genome to become accessible for biological processes such as transcription. The SWI/SNF chromatin remodeler is also one of the most frequently altered protein complexes in cancer, with upwards of 20% of all cancers carrying mutations in a SWI/SNF subunit. Intense studies over the last decade have probed the molecular events associated with SWI/SNF dysfunction in cancer and common themes are beginning to emerge in how tumor-associated SWI/SNF mutations promote malignancy. In this review, we summarize current understanding of SWI/SNF complexes, their alterations in cancer, and what is known about the impact of these mutations on tumor-relevant transcriptional events. We discuss how enhancer dysregulation is a common theme in SWI/SNF mutant cancers and describe how resultant alterations in enhancer and super-enhancer activity conspire to block development and differentiation while promoting stemness and self-renewal. We also identify a second emerging theme in which SWI/SNF perturbations intersect with potent oncoprotein transcription factors AP-1 and MYC to drive malignant transcriptional programs.
    Language English
    Publishing date 2022-07-26
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2516-8657
    ISSN (online) 2516-8657
    DOI 10.1177/25168657221115656
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Super-Enhancer Dysregulation in Rhabdoid Tumor Cells Is Regulated by the SWI/SNF ATPase BRG1.

    Jones, Cheyenne A / Wang, Jing / Evans, James R / Sisk, Hannah R / Womack, Carl B / Liu, Qi / Tansey, William P / Weissmiller, April M

    Cancers

    2024  Volume 16, Issue 5

    Abstract: Mutations in the SWI/SNF chromatin remodeling complex occur in ~20% of cancers. In rhabdoid tumors defined by loss of the SWI/SNF ... ...

    Abstract Mutations in the SWI/SNF chromatin remodeling complex occur in ~20% of cancers. In rhabdoid tumors defined by loss of the SWI/SNF subunit
    Language English
    Publishing date 2024-02-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16050916
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: WDR5 facilitates recruitment of N-MYC to conserved WDR5 gene targets in neuroblastoma cell lines.

    Bumpous, Leigh A / Moe, Kylie C / Wang, Jing / Carver, Logan A / Williams, Alexandria G / Romer, Alexander S / Scobee, Jesse D / Maxwell, Jack N / Jones, Cheyenne A / Chung, Dai H / Tansey, William P / Liu, Qi / Weissmiller, April M

    Oncogenesis

    2023  Volume 12, Issue 1, Page(s) 32

    Abstract: Collectively, the MYC family of oncoprotein transcription factors is overexpressed in more than half of all malignancies. The ability of MYC proteins to access chromatin is fundamental to their role in promoting oncogenic gene expression programs in ... ...

    Abstract Collectively, the MYC family of oncoprotein transcription factors is overexpressed in more than half of all malignancies. The ability of MYC proteins to access chromatin is fundamental to their role in promoting oncogenic gene expression programs in cancer and this function depends on MYC-cofactor interactions. One such cofactor is the chromatin regulator WDR5, which in models of Burkitt lymphoma facilitates recruitment of the c-MYC protein to chromatin at genes associated with protein synthesis, allowing for tumor progression and maintenance. However, beyond Burkitt lymphoma, it is unknown whether these observations extend to other cancers or MYC family members, and whether WDR5 can be deemed as a "universal" MYC recruiter. Here, we focus on N-MYC amplified neuroblastoma to determine the extent of colocalization between N-MYC and WDR5 on chromatin while also demonstrating that like c-MYC, WDR5 can facilitate the recruitment of N-MYC to conserved WDR5-bound genes. We conclude based on this analysis that N-MYC and WDR5 colocalize invariantly across cell lines at predicted sites of facilitated recruitment associated with protein synthesis genes. Surprisingly, we also identify N-MYC-WDR5 cobound genes that are associated with DNA repair and cell cycle processes. Dissection of chromatin binding characteristics for N-MYC and WDR5 at all cobound genes reveals that sites of facilitated recruitment are inherently different than most N-MYC-WDR5 cobound sites. Our data reveals that WDR5 acts as a universal MYC recruiter at a small cohort of previously identified genes and highlights novel biological functions that may be coregulated by N-MYC and WDR5 to sustain the neuroblastoma state.
    Language English
    Publishing date 2023-06-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2674437-5
    ISSN 2157-9024
    ISSN 2157-9024
    DOI 10.1038/s41389-023-00477-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The SWI/SNF ATPase BRG1 facilitates multiple pro-tumorigenic gene expression programs in SMARCB1-deficient cancer cells.

    Moe, Kylie C / Maxwell, Jack N / Wang, Jing / Jones, Cheyenne A / Csaki, Grace T / Florian, Andrea C / Romer, Alexander S / Bryant, Daniel L / Farone, Anthony L / Liu, Qi / Tansey, William P / Weissmiller, April M

    Oncogenesis

    2022  Volume 11, Issue 1, Page(s) 30

    Abstract: Malignant rhabdoid tumor (MRT) is driven by the loss of the SNF5 subunit of the SWI/SNF chromatin remodeling complex and then thought to be maintained by residual SWI/SNF (rSWI/SNF) complexes that remain present in the absence of SNF5. rSWI/SNF subunits ... ...

    Abstract Malignant rhabdoid tumor (MRT) is driven by the loss of the SNF5 subunit of the SWI/SNF chromatin remodeling complex and then thought to be maintained by residual SWI/SNF (rSWI/SNF) complexes that remain present in the absence of SNF5. rSWI/SNF subunits colocalize extensively on chromatin with the transcription factor MYC, an oncogene identified as a novel driver of MRT. Currently, the role of rSWI/SNF in modulating MYC activity has neither been delineated nor has a direct link between rSWI/SNF and other oncogenes been uncovered. Here, we expose the connection between rSWI/SNF and oncogenic processes using a well-characterized chemical degrader to deplete the SWI/SNF ATPase, BRG1. Using a combination of gene expression and chromatin accessibility assays we show that rSWI/SNF complexes facilitate MYC target gene expression. We also find that rSWI/SNF maintains open chromatin at sites associated with hallmark cancer genes linked to the AP-1 transcription factor, suggesting that AP-1 may drive oncogenesis in MRT. Interestingly, changes in MYC target gene expression are not overtly connected to the chromatin remodeling function of rSWI/SNF, revealing multiple mechanisms used by rSWI/SNF to control transcription. This work provides an understanding of how residual SWI/SNF complexes may converge on multiple oncogenic processes when normal SWI/SNF function is impaired.
    Language English
    Publishing date 2022-06-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2674437-5
    ISSN 2157-9024
    ISSN 2157-9024
    DOI 10.1038/s41389-022-00406-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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